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Ischemic stroke is a prominent contributor to global morbidity and mortality rates. The intricate and diverse mechanisms underlying ischemia–reperfusion injury remain poorly comprehended. RNA methylation, an emerging epigenetic modification, plays a crucial role in regulating numerous biological processes, including immunity, DNA damage response, tumorigenesis, metastasis, stem cell renewal, adipocyte differentiation, circadian rhythms, cellular development and differentiation, and cell division. Among the various RNA modifications, N6-methyladenosine (m6A) modification stands as the most prevalent in mammalian mRNA. Recent studies have demonstrated the crucial involvement of m6A modification in the pathophysiological progression of ischemic stroke. This review aims to elucidate the advancements in ischemic stroke-specific investigations pertaining to m6A modification, consolidate the underlying mechanisms implicated in the participation of m6A modification during the onset of ischemic stroke, and deliberate on the potential of m6A modification as a viable therapeutic target for ischemic stroke. [ABSTRACT FROM AUTHOR]

Noninvasive and effortless diagnosis of Alzheimer's disease (AD) remains challenging. Here we report the multiplexed profiling of extracellular vesicle (EV) surface proteins at the single EV level in five types of easily accessible body fluids using a proximity barcoding assay (PBA). A total of 183 surface proteins were detected on the EVs from body fluids collected from APP/PS1 transgenic mice and patients with AD. The AD‐associated differentially expressed EV proteins could discriminate between the control and AD/AD model samples with high accuracy. Based on machine learning predictive models, urinary EV proteins exhibited the highest diagnostic potential compared to those on other biofluid EVs, both in mice and humans. Single EV analysis further revealed AD‐associated EV subpopulations in the tested body fluids, and a urinary EV subpopulation with the signature proteins PLAU, ITGAX and ANXA1 could diagnose patients with AD in blinded datasets with 88% accuracy. Our results suggest that EVs and their subpopulations from noninvasive body fluids, particularly urine, are potential diagnostic biomarkers for AD. [ABSTRACT FROM AUTHOR]

In order to effectively prevent the occurrence of risky accidents during bridge construction, this study proposes a bridge construction risk assessment method based on variable weight theory and the cloud model theory. Firstly, the fishbone diagram was used to identify risk factors in constructing a bridge construction risk index system. Secondly, according to the cloud model theory, the comment cloud model of each risk index was established by using the forward cloud generator. Finally, the risk factor weights were quantified according to the intuitionistic fuzzy analytic hierarchy process (IFAHP). Combined with the variable weight theory, a zoning variable weight function was constructed and the weights were reallocated. Through the mutual aggregation of the comment cloud model and weights, the risk level of construction bridges was obtained. The method takes full account of the fuzziness and randomness existing in the evaluation process, optimizes the distribution of weight values of indicators, and uses Delphi iteration to effectively eliminate the subjective defects of individuals. A construction bridge in Changchun was used as an example for risk assessment, and the advance of the method was well verified. The results demonstrate that the method is highly feasible and effective after accuracy verification and sensitivity analysis. [ABSTRACT FROM AUTHOR]

Background: Patients with severe thalassemia may experience adverse effects from transfusion such as fever, rash, and iron overload after long-term transfusion therapy. Severe headaches as a side effect of blood transfusion in patients with thalassemia are not commonly observed, especially when combined with superficial siderosis of the central nervous system, which is easily misdiagnosed and requires excessive examination and treatment. Case Presentation: A 31-year-old woman was admitted with severe headache and vomiting over 3 days following blood transfusion. She was diagnosed with intermediate α-thalassemia at 2 years of age and had a history of irregular blood transfusions. Physical examination revealed horizontal nystagmus with no other abnormal neurological signs. Magnetic resonance (MR) imaging, MR venography, MR arteriography, and cerebrospinal fluid analysis were normal. However, susceptibility-weighted imaging showed abnormal signals in the bilateral and fourth ventricles. Initial antibiotics, antivirals, decompression of intracranial pressure, iron chelation, and symptomatic treatments were administered; subsequently, small intermittent blood transfusions were cautiously administered for severe anemia. The patient's headache was gradually relieved, and she was discharged on day 9. At the 5-month follow-up, the patient's headache recurred following another transfusion. Conclusions: Severe post-transfusion headache in patients with thalassemia has not been fully recognized and is easily misdiagnosed, leading to excessive examination and treatment. Understanding the clinical features of transfusion-related headaches can help identify this complication, but the exact pathophysiological mechanism requires further research. [ABSTRACT FROM AUTHOR]

Background: Patients with severe thalassemia may experience adverse effects from transfusion such as fever, rash, and iron overload after long-term transfusion therapy. Severe headaches as a side effect of blood transfusion in patients with thalassemia are not commonly observed, especially when combined with superficial siderosis of the central nervous system, which is easily misdiagnosed and requires excessive examination and treatment. Case Presentation: A 31-year-old woman was admitted with severe headache and vomiting over 3 days following blood transfusion. She was diagnosed with intermediate α-thalassemia at 2 years of age and had a history of irregular blood transfusions. Physical examination revealed horizontal nystagmus with no other abnormal neurological signs. Magnetic resonance (MR) imaging, MR venography, MR arteriography, and cerebrospinal fluid analysis were normal. However, susceptibility-weighted imaging showed abnormal signals in the bilateral and fourth ventricles. Initial antibiotics, antivirals, decompression of intracranial pressure, iron chelation, and symptomatic treatments were administered; subsequently, small intermittent blood transfusions were cautiously administered for severe anemia. The patient's headache was gradually relieved, and she was discharged on day 9. At the 5-month follow-up, the patient's headache recurred following another transfusion. Conclusions: Severe post-transfusion headache in patients with thalassemia has not been fully recognized and is easily misdiagnosed, leading to excessive examination and treatment. Understanding the clinical features of transfusion-related headaches can help identify this complication, but the exact pathophysiological mechanism requires further research. [ABSTRACT FROM AUTHOR]

The application of alkali sludge (derived from sodium silicate production) as a supplementary material for the cementitious system of alkali-activated slag was investigated through tests of mechanical strength, rheology, heat of hydration, and microscopic analysis. The enhanced alkali sludge dosage and alkali equivalent content increased the yield stress and plastic viscosity of the alkali-activated slag while decreasing the fluidity due to the better water absorption of the alkali sludge, which increased the flocculation of the particles. The compressive strength reached the maximum, with 30% alkali sludge and 7% alkali equivalent content. The addition of the alkali sludge postponed the formation of the hydrated calcium silicate (C-S-H) gel and, therefore, delayed the peak heat of hydration, but ultimately increased the total hydration heat release. The major hydration product of calcium silicate hydrate was found in the alkali-activated slag with a 10–30% blend of alkali sludge. This work provides a reference for the utilization of alkaline solid waste from the chemical industry as an alkali activator in cementitious construction materials. [ABSTRACT FROM AUTHOR]

Beta-2-microglobulin (B2M), cystatin C and lipocalin-2 (LCN-2) are established renal biomarkers, yet their roles in stroke have not been fully evaluated. We aimed to investigate the relationship of B2M, cystatin C, and LCN-2 with stroke risk in a general Chinese population. We used ordinal regression to study the relationship between serum B2M, cystatin C, and LCN-2 with stroke risk in 1060 participants (mean age 45.4 ± 10.8 years, 46% male) from the Shenzhen-Hong Kong United Network on Cardiovascular Disease (SHUN-CVD) study. Stroke risk was classified into low-risk, middle-risk and high-risk groups according to the China National Stroke Screening Survey criteria. Serum biomarker levels were measured using immunoturbidimetric assays. Participants with valid data on serum biomarker levels and stroke risk were included in the analysis. The number of participants in the low-risk, middle-risk and high-risk stroke risk groups were 663, 143 and 254 respectively. Elevated serum B2M, cystatin C, and LCN-2 levels were associated with being male, overweight/obesity, hypertension, alcohol consumption and smoking. Serum B2M, cystatin C and LCN-2 levels were significantly associated with stroke risk in the overall population (B2M: β = 0.595, p <.001; cystatin C: β = 3.718, p <.001; LCN-2: β = 0.564, p <.001) after adjustment for age. Elevated serum B2M, cystatin C and LCN-2 levels are associated with stroke risk. They may be novel biomarkers for clinicians to assess stroke risk. Serum beta-2-microglobulin, cystatin C and lipocalin-2 levels are significantly associated with stroke risk. Beta-2-microglobulin, cystatin C and lipocalin-2 may serve as useful biomarkers for stroke risk stratification in the general population. [ABSTRACT FROM AUTHOR]

Background: Hand knob infarction induced focal weakness of contralateral hand or distal arm, only accounts for less than 1% of all ischemic strokes. To date, there is no case with pain during sleep as the onset symptoms being reported. The atypical symptoms of hand knob infarction might increase the risk of delaying treatment especially in the hyperacute phase of stroke. Case presentation: A 70-year-old man awoke from sleep due to sudden pain of his right medial wrist and presented to the emergency department with difficulty extending his right index and middle fingers within the time window of intravenous thrombolysis. But the intravenous thrombolysis was not given based on the NIHSS score (0) and atypical symptoms. MRI showed multiple DWI hyperintense lesions, including partial left hand knob area and left posterior central gyrus. CTA showed a severe focal stenosis of proximal left internal carotid artery. Conclusions: The hand knob infarction might onset with unusual pain and should be carefully inspected in patients combined with acute onset of focal hand paresis. [ABSTRACT FROM AUTHOR]

Aims Chemoattractants and their cognate receptors are essential for leucocyte recruitment during atherogenesis, and atherosclerotic plaques preferentially occur at predilection sites of the arterial wall with disturbed flow (d-flow). In profiling the endothelial expression of atypical chemoattractant receptors (ACKRs), we found that Ackr5 (CCRL2) was up-regulated in an endothelial subpopulation by atherosclerotic stimulation. We therefore investigated the role of CCRL2 and its ligand chemerin in atherosclerosis and the underlying mechanism. Methods and results By analysing scRNA-seq data of the left carotid artery under d-flow and scRNA-seq datasets GSE131776 of ApoE−/− mice from the Gene Expression Omnibus database, we found that CCRL2 was up-regulated in one subpopulation of endothelial cells in response to d-flow stimulation and atherosclerosis. Using CCRL2−/−ApoE−/− mice, we showed that CCRL2 deficiency protected against plaque formation primarily in the d-flow areas of the aortic arch in ApoE−/− mice fed high-fat diet. Disturbed flow induced the expression of vascular endothelial CCRL2, recruiting chemerin, which caused leucocyte adhesion to the endothelium. Surprisingly, instead of binding to monocytic CMKLR1, chemerin was found to activate β2 integrin, enhancing ERK1/2 phosphorylation and monocyte adhesion. Moreover, chemerin was found to have protein disulfide isomerase-like enzymatic activity, which was responsible for the interaction of chemerin with β2 integrin, as identified by a Di-E-GSSG assay and a proximity ligation assay. For clinical relevance, relatively high serum levels of chemerin were found in patients with acute atherothrombotic stroke compared to healthy individuals. Conclusions Our findings indicate that d-flow-induced CCRL2 promotes atherosclerotic plaque formation via a novel CCRL2-chemerin-β2 integrin axis, providing potential targets for the prevention or therapeutic intervention of atherosclerosis. [ABSTRACT FROM AUTHOR]

Background: Subacute combined degeneration (SCD) is a demyelinating disease characterized by vitamin B12 deficiency related segmental degeneration of the dorsal or lateral columns of the spinal cord. However, few cases have been reported as a comorbidity of SCD and neuromyelitis optica spectrum disease (NMOSD).Case Presentation: Herein, we describe a female patient (61-year-old) who had sensory deficits, paresthesia, and weakness of the distal extremities for over 2 months. She then received an initial diagnosis of SCD with typical inverted "V-sigh" hyperintensities over the posterior aspect of the spinal cord in magnetic resonance imaging (MRI - T2-weighted imaging), as well as megaloblastic anaemia in blood examinations. From the past history, there was no evidence of a dietary deficiency or gastric abnormalities. However, traditional treatment with vitamin B12 supplementation was ineffective. Hence, a demyelinating antibody examination showed that she had antibodies targeting aquaporin 4 (AQP4) in both the cerebrospinal fluid and serum, leading to the diagnosis of NMOSD. Her clinical symptoms were obviously improved after treatment with intravenous glucocorticoids.Conclusion: People who have nutritional deficiency or altered gastrointestinal function are more likely to develop SCD. This case raises the awareness that the poor therapeutic effects of simple vitamin B12 supplementation could be explained by immunoreactions against AQP4. A better recognition will be of great importance for the correct diagnosis of the comorbidity, as well as for essential treatment and even a better prognosis. [ABSTRACT FROM AUTHOR]

Background: Existing data suggest that cerebral autoregulation (CA) varies among different subtypes of ischaemic stroke. CA is globally impaired in patients with small artery occlusion (SAO). However, the factors influencing CA impairment in patients remains to be elucidated.Methods: Stroke patients with SAO who underwent brain magnetic resonance imaging (MRI) were prospectively studied. Within 7 days after stroke onset, CA was recorded from the middle cerebral artery blood flow velocity and arterial blood pressure was simultaneously measured. Transfer function analysis was used to derive CA parameters, including gain and phase. Clinical characteristics, mean arterial pressure (MAP), biochemical findings, and cerebral small vessel disease (CSVD) markers on MRI were assessed in each patient. Factors associated with CA parameters were investigated. Univariate and multivariate linear regression analyses were conducted to determine the relationship between clinical factors and CA parameters.Results: Sixty-three SAO patients (age, 56.3 ± 9.9 years; 55 men) were enrolled in the study. In the multiple linear regression analysis, after controlling for relevant clinical factors, MAP on admission (ipsilateral OR = 0.99 and contralateral OR = 0.99, both P < 0.005) was a significant independent predictor of bilateral gain. MAP > 105 mmHg on admission (OR = 0.77, P = 0.019) was significantly associated with ipsilateral gain. Diabetes mellitus was a significant predictive factor for bilateral gain (ipsilateral OR = 1.32 and contralateral OR = 1.22, both P < 0.005). No correlations were found between CA parameters and CSVD characteristics.Conclusion: In SAO-related ischaemic stroke, patients with MAP > 105 mmHg on admission tended to have better ipsilateral CA. Diabetes mellitus appears to be an independent risk factor for CA impairment in patients with SAO-related stroke. CSVD may not be the main factor affecting bilateral CA in patients with SAO. [ABSTRACT FROM AUTHOR]

Glioblastoma multiforme (GBM) is the most common type of malignant brain tumor, among which IDH1-wild type GBM has a poor prognosis. Recent studies have shown that ferroptosis-related genes (FRGs) are correlated with the development and progression of cancer. In GBM, the role of FRGs associated with IDH1 status as biological indicators and therapeutic targets remains to be clarified. Ten of FRGs (STEAP3, HSPB1, MAP1LC3A, SOCS1, LOX, CAPG, CP, GDF15, CDKN1A, and CD44) associated with IDH1 status in GBM were identified as key genes through screening by survival analysis and Random Forest using The Cancer Genome Atlas (TCGA) datasets, and the protein expressions of key genes were verified. Transwell and qPCR results showed that ferroptosis promoted the migration of glioblastoma cells and affected the expression of key genes. Our study established the ferroptosis-related prognostic model for GBM patients based on ten key genes by a different modeling method from previous study, the GSVA algorithm. Further, we took the methods of functional enrichment analysis, clinical characteristics, immune cell infiltration, immunomodulator, ESTIMATE and single nucleotide variant (SNV) analysis to study the molecular mechanisms of prognostic model and key genes. The results showed that ten key genes were strongly associated with immune-related factors and were significantly involved in the p53 signaling pathway, senescence and autophagy in cancer, and in the negative regulation of protein kinase activity. Moreover, potential therapeutic drugs were identified by Virtual Screening and Molecular Docking. Our study indicated that the novel ferrotosis-related prognostic model for GBM patients and key genes possessed the prognostic and therapeutic values. [ABSTRACT FROM AUTHOR]

This article aims to explore the possible causal relationship between loneliness and depression in college students. Two hundred and fifty-nine college students had been investigated four times in 2 years with UCLA and CES-D, and cross-lagged regression analysis was used. ① there was a significant positive correlation between loneliness and depression of college students; ② cross-lagged regression analysis showed that after controlling the related variables and the stability of variables themselves, loneliness, and depression could positively predict each other at points-in-time T1 and T2; Depression could significantly positively predict loneliness at points-in-time T2, T3, and T4. There is a bidirectional relationship between loneliness and depression of college students, and the effect of depression on loneliness is stronger than that of loneliness on depression. [ABSTRACT FROM AUTHOR]

Background: Progressive encephalomyelitis with rigidity and myoclonus (PERM) is an acute, potentially life-threatening, yet curable neuro-immunological disease characterized by spasms, muscular rigidity, and brainstem and autonomic dysfunction. The clinical features of glycine receptor (GlyR) antibody-positive PERM may be overlooked, particularly with some unusual symptoms.Case Presentation: A 52-year-old man was admitted to the hospital for evaluation of tension headache for 20 days and mild dysarthria. These symptoms were followed by panic, profuse sweating, severe dysarthria, dizziness, unsteady gait, and paroxysmal muscle spasms. Brain magnetic resonance imaging and cerebrospinal fluid analysis were normal. The patient's condition steadily deteriorated. He repeatedly presented with rigidity, panic attacks, severe anxiety, paroxysmal inspiratory laryngeal stridor, cyanosis of the lips, and intractable epilepsy. Electromyography showed multiple myoclonic seizures, a single generalized tonic-clonic seizure, and a single generalized tonic seizure. Screening for autoimmune encephalitis antibodies revealed anti-GlyR antibodies in his cerebrospinal fluid. Immunomodulatory pulse therapy with steroids and immunoglobulin resulted in expeditious improvement of the symptoms within 2 weeks, and a follow-up at 5 weeks showed consistent clinical improvement.Conclusion: Our case highlights that inspiratory laryngeal stridor is an important symptom of PERM. Our observation widens the spectrum of the clinical presentation of anti-GlyR antibody-positive PERM, where early identification is a key to improving prognosis. [ABSTRACT FROM AUTHOR]

Background: Ischaemic stroke and transient ischaemic attack (TIA) share a common cause. We aim to develop and validate a concise prognostic nomogram for patients with minor stroke and TIA.Methods: A total of 994 patients with minor stroke and TIA were included. They were split into a derivation (n=746) and validation (n=248) cohort. The modified Rankin Scale (mRS) scores 3 months after onset were used to assess the prognosis as unfavourable outcome (mRS≥2) or favourable outcome (mRS<2).Result: The final model included seven independent predictors: gender, age, baseline National Institute of Health Stroke Scale (NIHSS), hypertension, diabetes mellitus, white blood cell and serum uric acid. The Harrell's concordance index (C-index) of the nomogram for predicting the outcome was 0.775 (95% CI 0.735 to 0.814), which was confirmed by the validation cohort (C-index=0.787 (95% CI 0.722 to 0.853)). The calibration curve showed that the nomogram-based predictions were consistent with actual observation in both derivation cohort and validation cohort.Conclusion: The proposed nomogram showed favourable predictive accuracy for minor stroke and TIA. This has the potential to contribute to clinical decision-making. [ABSTRACT FROM AUTHOR]

Background: Qualitative research can reflect the actual thoughts and experience of research subjects and can be used to explore the experiences of women presenting with twin-to-twin transfusion syndrome (TTTS) to facilitate the provision of targeted psychological support.Methods: A semi-structured interview method was used to assess the pregnancy and parenting experiences of women with TTTS. Colaizzi method was used for data analysis.Results: Eighteen women participated in the study. We found that women with TTTS during pregnancy experienced persistent worry about their children's health from the disease diagnosis to the subsequent parenting processes, even in case of minor changes in their children's health. The lack of an efficient referral process and health information increased their uncertainty about their children's health.Conclusion: In addition to the children's health, other difficulties encountered during pregnancy and parenting may aggravate the pressure. Clinicians in the first-visit hospital and foetal medicine centre should improve the referral process and establish a follow-up system to provide women with health information and psychological support. [ABSTRACT FROM AUTHOR]

Electroencephalographic (EEG) neurofeedback (NFB) is a popular neuromodulation method to help one selectively enhance or inhibit his/her brain activities by means of real-time visual or auditory feedback of EEG signals. Sensory motor rhythm (SMR) NFB protocol has been applied to improve cognitive performance, but a large proportion of participants failed to self-regulate their brain activities and could not benefit from NFB training. Therefore, it is important to identify the neural predictors of SMR up-regulation NFB training performance for a better understanding the mechanisms of individual difference in SMR NFB. Twenty-seven healthy participants (12 males, age: 23.1 ± 2.36) were enrolled to complete three sessions of SMR up-regulation NFB training and collection of multimodal neuroimaging data [resting-state EEG, structural magnetic resonance imaging (MRI), and resting-state functional MRI (fMRI)]. Correlation analyses were performed between within-session NFB learning index and anatomical and functional brain features extracted from multimodal neuroimaging data, in order to identify the neuroanatomical and neurophysiological predictors for NFB learning performance. Lastly, machine learning models were trained to predict NFB learning performance using features from each modality as well as multimodal features. According to our results, most participants were able to successfully increase the SMR power and the NFB learning performance was significantly correlated with a set of neuroimaging features, including resting-state EEG powers, gray/white matter volumes from MRI, regional and functional connectivity (FC) of resting-state fMRI. Importantly, results of prediction analysis indicate that NFB learning index can be better predicted using multimodal features compared with features of single modality. In conclusion, this study highlights the importance of multimodal neuroimaging technique as a tool to explain the individual difference in within-session NFB learning performance, and could provide a theoretical framework for early identification of individuals who cannot benefit from NFB training. [ABSTRACT FROM AUTHOR]

Background: T2-weighted (T2w) intracranial vessel wall imaging (IVWI) provides good contrast to differentiate intracranial vasculopathies and discriminate various important plaque components. However, the strong cerebrospinal fluid (CSF) signal in T2w images interferes with depicting the intracranial vessel wall. In this study, we propose a T2-prepared sequence for whole-brain IVWI at 3T with CSF suppression. Methods: A preparation module that combines T2 preparation and inversion recovery (T2IR) was used to suppress the CSF signal and was incorporated into the commercial three-dimensional (3D) turbo spin echo sequence-Sampling Perfection with Application optimized Contrast using different flip angle Evolution (SPACE). This new technique (hereafter called T2IR-SPACE) was evaluated on nine healthy volunteers and compared with two other commonly used 3D T2-weighted sequences: T2w-SPACE and FLAIR-SPACE (FLAIR: fluid-attenuated inversion recovery). The signal-to-noise ratios (SNRs) of the vessel wall (VW) and CSF and contrast-to-noise ratios (CNRs) between them were measured and compared among these three T2-weighted sequences. Subjective wall visualization of the three T2-weighted sequences was scored blindly and independently by two radiologists using a four-point scale followed by inter-rater reproducibility analysis. A pilot study of four stroke patients was performed to preliminarily evaluate the diagnostic value of this new sequence, which was compared with two conventional T2-weighted sequences. Results: T2IR-SPACE had the highest CNR (11.01 ± 6.75) compared with FLAIR-SPACE (4.49 ± 3.15; p < 0.001) and T2w-SPACE (−56.16 ± 18.58; p < 0.001). The subjective wall visualization score of T2IR-SPACE was higher than those of FLAIR-SPACE and T2w-SPACE (T2IR-SPACE: 2.35 ± 0.59; FLAIR-SPACE: 0.52 ± 0.54; T2w-SPACE: 1.67 ± 0.58); the two radiologists' scores showed excellent agreement (ICC = 0.883). Conclusion: The T2IR preparation module markedly suppressed the CSF signal without much SNR loss of the other tissues (i.e., vessel wall, white matter, and gray matter) compared with the IR pulse. Our results suggest that T2IR-SPACE is a potential alternative T2-weighted sequence for assessing intracranial vascular diseases. [ABSTRACT FROM AUTHOR]

Objective: Previous studies suggested that insomnia was associated with an increased risk of cardiocerebral vascular diseases (CVDs) but not clear in different insomnia symptoms. We performed a meta-analysis to investigate the association of individual insomnia symptoms and risk of CVDs. Methods: In this meta-analysis, we systematically searched published articles by using electronic databases including PubMed, Cochrane Library, MedLine, and Google Scholar. Studies were enrolled if they indicated clear insomnia symptoms, prospective, and evaluated the association of insomnia symptoms and CVD outcome in adults free of CVDs at baseline. Results: There were seven prospective cohort studies with sample sizes ranging from 2,960 to 487,200 included in this meta-analysis. Mean follow-up duration was 10.6 years. Insomnia symptoms of having difficulty initiating or maintaining sleep (DIS or DMS), non-restorative sleep (NRS), and early morning awakening (EMA) were analyzed in this study. All studies were compared under a random-effects model. NRS, DIS, and DMS were, respectively, related to 16% [hazard ratio (HR) 1.16, 95% CI 1.07–1.24], 22% (HR 1.22, 95% CI 1.06–1.40), and 14% (HR 1.14, 95% CI 1.02–1.27) higher risk of first-ever CVD incidence during the follow-up. Based on our analysis, EMA was not a risk factor of CVDs (HR 1.06, 95% CI 0.99–1.13). Conclusion: This study suggested that symptoms of DIS, DIM, or NRS were associated with a higher risk of CVD incidence in insomnia patients free of CVDs at baseline. But this association was not significant in insomnia patients complaining about EMA. [ABSTRACT FROM AUTHOR]

This study aims to explore the moderating role of affinity for aloneness and gender in the relationship between loneliness and depression. Methods: The University of California at Los Angeles (UCLA) loneliness scale, the Loneliness and Aloneness Scale for Children and Adolescents (LACA), and the Centre for Epidemiologic Studies Depression Scale (CES-D) were administered for 831 college students (317 males and 460 females). Results: (1) Males had higher scores than females for loneliness and depression. (2) Loneliness was positively associated with affinity for aloneness and depression, whereas affinity for aloneness was positively associated with depression. (3) The moderating effects of affinity for aloneness in the correlation between loneliness and depression only existed in males, and affinity for aloneness can buffer the effect of loneliness on depression. Results: Affinity for aloneness may be a buffering factor that serves to protect individuals with high loneliness from developing psychological problems, especially among males. [ABSTRACT FROM AUTHOR]

Purpose: To explore the effect of SEV on colon cancer cells through circ-PI4KA. Methods: The RNA level of circular RNA_0062389, microRNA-331-3p and LIM and SH3 protein 1 was determined by quantitative real-time polymerase chain reaction. Protein expression was detected by Western blot. Cell proliferation was investigated by 3-(4,5)-dimethylthiahiazo (-z-y1)-3,5-di-phenytetrazoliumromide, cell colony formation and 5-ethynyl-29-deoxyuridine assays. Cell apoptosis was demonstrated using Annexin V-fluorescein isothiocyanate/propidium iodide double staining assay. Cell migration and invasion were detected by transwell assay. The target relationship between miR-331-3p and circ-PI4KA or LASP1 was predicted by starBase v2.0 online database, and identified by a dual-luciferase reporter assay. The effects between SEV treatment and circ-PI4KA knockdown on tumor formation were presented by in vivo tumor formation assay. Results: Circ-PI4KA and LASP1 expressions were dramatically upregulated, while miR-331-3p was downregulated in colon cancer tissues and cells, respectively. SEV exposure significantly decreased the expression of circ-PI4KA and LASP1, but increased miR-331-3p expression. SEV inhibited cell proliferation, migration and invasion, and induced cell apoptosis by regulating circ-PI4KA. Furthermore, circ-PI4KA interacted with miR-331-3p, and miR-331-3p interacted with LASP1. SEV inhibited tumor growth by controlling circ-PI4KA in vivo. Conclusion: Circ-PI4KA attenuated SEV-treated colon cancer cell malignancy by upregulating LASP1 through binding to miR-331-3p, which provided a new mechanism for studying surgery-mediated therapy of colon cancer. [ABSTRACT FROM AUTHOR]

Background: Anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis (AE) is a common cause of nonviral infectious encephalitis, which can be triggered by herpes simplex virus infection. Previous studies have shown that approximately 27% of herpes simplex encephalitis (HSE) patients produce anti-NMDAR antibodies within 3 months. Immunotherapy is recommended in this situation, but some symptoms usually remain in the 1-year follow-up. Case presentation: A previously healthy 23-year-old Chinese young woman developed epileptic attack followed by psychiatric symptoms of confusion and irritation as well as cognitive deficits. Brain MRI showed hyperintense lesions of the right temporal lobe on DWI and T2 without contrast enhancement effects. Twenty-one days of acyclovir was administered based on the primary diagnosis of HSE. The anti-NMDAR antibody (IgG) was detected positively on day 11 after disease onset. She had improved cognitive function but suffered another grand mal epilepsy after the first course of intravenous immunoglobulin (IVIG) therapy combined with 1000 mg intravenous methylprednisolone. After discussion, another course of IVIG was started for 5 days. Her symptoms were well controlled with only mild cognitive deficits at the 1-year follow-up (mRS = 1). Conclusions: Our case indicated that anti-NMDAR antibodies could develop earlier after HSE compared with previous data from adults. We suggested detecting AE antibodies simultaneously with each CSF analysis. Meanwhile, the second course of IVIG therapy was reasonable when symptoms were not controlled after the first course of IVIG combined with IV steroid treatment. [ABSTRACT FROM AUTHOR]

Background: During medical imaging, cystic radiation encephalopathy and brain metastasis are difficult to differentiate, and hence they are easily misdiagnosed. To our knowledge, a nasopharyngeal carcinoma recurrence after more than seven years with cerebral metastasis that mimicked cystic radiation encephalopathy has not been reported.Case Presentation: A 52-year-old man was admitted to the hospital owing to weakness of the right limb for one month, which increased in intensity for three days. He had been diagnosed with nasopharyngeal carcinoma in 2011, which was treated by radiotherapy. The patient successively developed cystic radiation encephalopathy and brain metastasis from the nasopharyngeal carcinoma, which mimicked cystic radiation encephalopathy relapse. Left frontotemporal craniotomy, surgical resection of brain metastasis, and repair of the skull base and dura were performed. Postoperative computed tomography showed that midline deviation recovered, and brain edema was reduced.Conclusions: This report is significant because brain metastasis from nasopharyngeal carcinoma can masquerade as a benign entity and cause fatal consequences. In patients presenting with cystic radiation encephalopathy, brain metastasis should be considered as a differential diagnosis. [ABSTRACT FROM AUTHOR]

Protein disulphide isomerase (PDI) promotes platelet activation and constitutes a novel antithrombotic target. In this study, we reported that a PDI‐binding plant polyphenol, tannic acid (TA), inhibits PDI activity, platelet activation and thrombus formation. Molecular docking using plant polyphenols from dietary sources with cardiovascular benefits revealed TA as the most potent binding molecule with PDI active centre. Surface plasmon resonance demonstrated that TA bound PDI with high affinity. Using Di‐eosin‐glutathione disulphide fluorescence assay and PDI assay kit, we showed that TA inhibited PDI activity. In isolated platelets, TA inhibited platelet aggregation stimulated by either GPVI or ITAM pathway agonists. Flow cytometry showed that TA inhibited thrombin‐ or CRP‐stimulated platelet activation, as reflected by reduced granule secretion and integrin activation. TA also reduced platelet spreading on immobilized fibrinogen and platelet adhesion under flow conditions. In a laser‐induced vascular injury mouse model, intraperitoneal injection of TA significantly decreased the size of cremaster arteriole thrombi. No prolongation of mouse jugular vein and tail‐bleeding time was observed after TA administration. Therefore, we identified TA from natural polyphenols as a novel inhibitor of PDI function. TA inhibits platelet activation and thrombus formation, suggesting it as a potential antithrombotic agent. [ABSTRACT FROM AUTHOR]

Carotid plaque neovascularization is one of the major factors for the classification of vulnerable plaque, but the axial force effects of the pulsatile blood flow on the plaque with neovessel and intraplaque hemorrhage was unclear. Together with the severity of stenosis, the fibrous cap thickness, large lipid core, and the neovascularization followed by intraplaque hemorrhage (IPH) have been regarded as high-risk features of plaque rupture. In this work, the effects of these factors were evaluated on the progression and rupture of the carotid atherosclerotic plaques. Five geometries of carotid artery plaque were developed based on contrast-enhanced ultrasound (CEUS) images, which contain two types of neovessel and IPH, and geometry without neovessel and IPH. A one-way fluid-structure interaction model was applied to compute the maximum principal stress and strain in the plaque. For that hyper-elastic and non-linear material, Yeoh 3rd Order strain energy density function was used for components of the plaque. The simulation results indicated that the maximum principal stress of plaque in the carotid artery was higher when the degree of the luminal stenosis increased and the thickness of the fibrous cap decreased. The neovessels within the plaque could introduce a 2.5% increments of deformation in the plaque under the pulsatile blood flow pressure. The IPH also contributed to the increased risk of plaque rupture that a gain of stress was 8.983, 14.526, and 34.47 kPa for the plaque with 50, 65, and 75%, respectively, when comparing stress in the plaque with IPH distributed at the middle to the shoulder of the plaque. In conclusion, neovascularization in the plaque could reduce the stability of the plaque by increasing the stress within the plaque. Also, the risk of plaque rupture increased when large luminal stenosis, thin fibrous cap, and IPH were observed. [ABSTRACT FROM AUTHOR]

Background: Intracranial arterial calcification (IAC) is highly prevalent in ischemic stroke patients. However, data on the association of IAC with stroke recurrence and mortality remains limited. We examined the effect of IAC on the long-term recurrence of stroke and the risk of post-stroke mortality. Methods: Using a prospective stroke registry, we recruited 694 patients (mean age 71.6 ± 12.4; male sex 50.3%) since December 2004. IAC was visualized using the computed tomography exam that was made at hospital admission and was quantified with the Agatston method. All patients were regularly followed up till July 2016. The impacts of IAC on stroke recurrence and mortality were assessed using Cox-regression models with adjustments for age, sex, and relevant cardiovascular risk factors. Results: During a median follow-up period of 8.8 years, 156 patients (22.5%) suffered a recurrent stroke and 84 died (12.1%). We found that a higher IAC Agatston score related to a higher risk of stroke recurrence (HR per 1-SD increase in IAC: 1.30; 95% CI, 1.08–1.56, p = 0.005) and a higher risk of post-stroke mortality (HR per 1-SD increase, 1.44; 95% CI, 1.06–1.96, p = 0.019). After investigating etiology-specific risks of stroke-recurrence, we found that a higher IAC Agatston score specifically associated with small-vessel occlusive stroke. Conclusions: IAC is a strong risk factor for recurrent stroke and post-stroke mortality. Among stroke subtypes, IAC relates to higher risk of stroke recurrence among patients with small-vessel disease, which indicates chronic calcification detected in large cerebral arteries may have potential effects on the cerebrovascular beds extending to small vessels. [ABSTRACT FROM AUTHOR]

HNG, a highly potent mutant of the anti‐Alzheimer peptide‐humanin, has been shown to protect against ischaemia‐reperfusion (I/R) injury. However, the underlying mechanism related to platelet activation remains unknown. We proposed that HNG has an effect on platelet function and thrombus formation. In this study, platelet aggregation, granule secretion, clot retraction, integrin activation and adhesion under flow conditions were evaluated. In mice receiving HNG or saline, cremaster arterial thrombus formation induced by laser injury, tail bleeding time and blood loss were recorded. Platelet microtubule depolymerization was evaluated using immunofluorescence staining. Results showed that HNG inhibited platelet aggregation, P‐selectin expression, ATP release, and αIIbβ3 activation and adhesion under flow conditions. Mice receiving HNG had attenuated cremaster arterial thrombus formation, although the bleeding time was not prolonged. Moreover, HNG significantly inhibited microtubule depolymerization, enhanced tubulin acetylation in platelets stimulated by fibrinogen or microtubule depolymerization reagent, nocodazole, and inhibited AKT and ERK phosphorylation downstream of HDAC6 by collagen stimulation. Therefore, our results identified a novel role of HNG in platelet function and thrombus formation potentially through stabilizing platelet microtubules via tubulin acetylation. These findings suggest a potential benefit of HNG in the management of cardiovascular diseases. [ABSTRACT FROM AUTHOR]

Objectives: To compare visualization of joint intracranial and carotid vessel walls between 5× compressed sensing accelerated three-dimensional DANTE-SPACE sequence (CS VWI) acquired in 5 min and the same sequence accelerated by 2.7× parallel imaging (PI VWI) which takes 9–10 min currently. Methods: Following institutional review board approval and informed consent, 28 subjects including 20 stroke patients underwent PI and CS VWI examinations with an acquired spatial resolution of isotropic 0.55 mm and joint coverage of intracranial and carotid arteries. Quantitative wall thickness measurements of CS VWI and PI VWI were compared on healthy volunteers and patients with wall thickening respectively. Subjective wall visualizations of the two VWI methods on patients were scored by two radiologists blindly and independently using a 4-point scale followed by inter-rater reproducibility analysis. Results: Linear regression analysis of wall thickness measurements showed excellent agreement between CS VWI and PI VWI in both healthy volunteers (r = 0.99) and stroke patients with wall thickening (r = 0.99). Subjective wall visualization score of CS VWI was slightly lower than PI VWI (3.13 ± 0.41 vs. 3.31 ± 0.79) but still had good diagnostic quality (> 3 based on a 4-point scale). The two radiologists' scores agreed excellently, evidenced by the intraclass correlation coefficient (ICC) values being higher than 0.75 (p < 0.001). Conclusions: Compressed sensing expedients joint intracranial and carotid VWI acquired at an isotropic resolution of 0.55 mm in 5 min without compromising quantitative vessel wall thickness measurement or diagnostic wall visualization. Key Points: • CS VWI facilitates comprehensive visualization of intracranial and carotid vessel walls at an acquired isotropic resolution of 0.55 mm in a single 5-min scan. • CS VWI affords comparable vessel wall visualization and morphology measurement as PI VWI with a shortened acquisition time by 45%. • CS VWI alleviates the intensive trade-off between imaging resolution and scan time, and benefits the scan efficiency, motion robustness, and patient tolerance of high-resolution joint intracranial and carotid VWI. [ABSTRACT FROM AUTHOR]

Objective: To evaluate the relationship between contrast-enhanced ultrasonography (CEUS) of carotid intraplaque neovascularization and ischemic stroke in transient ischemic attack (TIA) patients. Methods: A total of 112 TIA patients were selected for the study. Routine carotid ultrasonic examination was performed for all the patients. CEUS was carried out for consecutive patients with plaque thicker than 2.5 mm in carotid bifurcation and follow-up for at least 24 months. The number of patients with incurrence of ischemic stroke or recurrence of TIA was obtained during the follow-up period. To detect the risk factors for incurrence of ischemic stroke or recurrence of TIA in 24 months, multivariate logistic regression analyses were performed for all the risk factors in all the selected patients. Results: Ninety-one patients underwent CEUS and were followed up at least 24 months. There were statistical differences between recurrent and non-recurrent groups about hypertension, diabetes, hyperlipemia, smoking history, family history of stroke, medication compliance, two-dimensional ultrasound, and CEUS (P < 0.05). The higher CEUS intensity in the carotid plaque was, the higher was the possibility of ischemic stroke or recurrent TIA. Multivariate logistic regression analysis showed that the CEUS characteristics of carotid plaque such as linear enhancement or diffuse enhancement were independent risk factors for ischemic stroke or recurrent TIA in TIA patients (P < 0.05). Conclusion: For carotid plaques, CEUS could evaluate the infusion mode, which could reflect the neovascularization in plaques. CEUS could predict the incurrence of ischemic stroke or recurrence of TIA in TIA patients, which is useful information when making a clinical decision. [ABSTRACT FROM AUTHOR]

Semaphorin 7A (Sema7A), a neural guidance cue, was recently identified to regulate atherosclerosis in mice. However, the clinical relevance of Sema7A with atherosclerotic diseases remains unknown. The aim of this study was to investigate the association between serum Sema7A and the risk of acute atherothrombotic stroke (AAS). We measured serum concentrations of Sema7A in 105 newly onset AAS cases and 105 age‐ and sex‐matched controls, showing that median Sema7A level in AAS cases was over three times of that in controls (5.86 vs 1.66 ng/mL). Adjusted for hypertension, body mass index, fasting blood glucose, total cholesterol, triglyceride, high‐density lipoprotein (HDL)‐cholesterol, low‐density lipoprotein (LDL)‐cholesterol, current smoking and alcohol consumption, multivariate logistic regression showed that higher Sema7A was independently associated with the odds of AAS (OR = 6.40, 95% CI: 2.88‐14.25). Each 1‐standard deviation increase in Sema7A was associated with a threefold higher odds of AAS (OR = 3.42, 95% CI: 1.84‐6.35). Importantly, adding Sema7A to a multivariate logistic model containing conventional cardiovascular risk factors improved the area under receiver operating characteristic curves from 0.831 to 0.891 for the association with AAS. In conclusion, elevated serum Sema7A is independently associated with the risk of AAS, suggesting that it may play a potential role in AAS. [ABSTRACT FROM AUTHOR]

Introduction: Lipoprotein-associated phospholipase A2 (Lp-PLA2) is a well-known risk factor of atherosclerotic vascular diseases. Nevertheless, its role in the acute phase of ischemic stroke is still unclear. The aim of this study is to identify the relationship between Lp-PLA2 levels and early neurological deterioration (END) in acute ischemic stroke patients with Trial of Org 10 172 in Acute Stroke Treatment (TOAST) subtype of large arterial atherosclerosis (LAA). Methods: We enrolled Chinese patients with first ever acute ischemic stroke admitted to Neurology Department of Shenzhen Second People's Hospital within 48 h from onset of symptoms during January - November 2015. Demographic and laboratory information were collected while END was defined as an increase in the National Institute of Health Stroke Scale score by ≥ 1 point in motor power, or ≥ 2 points in the total score within 10 days after admission. Results: Overall 181 patients were involved; END was diagnosed in 30 patients within 10 days after admission. The odds ratio for END increased with increasing levels of Lp-PLA2 (intermediate level, OR = 1.96, 95%CI 1.02-4.27, p = 0.041; high level, OR = 2.99, 95%CI 1.26-5.73, p = 0.023). Conclution: Intermediate and high level of Lp-PLA2 was identified as independent predictor of END in multivariate analysis. Lp-PLA2 could be valued as a risk factor of END in patients with acute ischemic stroke with TOAST subtype of LAA. [ABSTRACT FROM AUTHOR]

Abstract: In order to improve the detonation performances of emulsion explosives, a new type of emulsion explosives sensitized by hydrogen‐storage glass microballoons is proposed. The influences of hydrogen in glass microballoons on explosion characteristics of emulsion explosives were studied. Brisance testing and underwater explosion experiments showed that, compared with traditional emulsion explosives, the shock impulse and specific total energy of hydrogen‐storage glass microballoons sensitized emulsion explosives are improved significantly. The brisance (compression of lead block) of hydrogen‐storage emulsion explosives is 23.0 mm, 3.2 mm more than that of traditional emulsion explosives. Therefore, the hydrogen‐storage glass microballoons could be a promising energetic additive for developing high‐power emulsion explosives. [ABSTRACT FROM AUTHOR]

Experiments were conducted to study the underwater explosion performance of titanium hydride/RDX-based (TiH2/RDX) composite explosive. Cylinder charges with different TiH2 particle sizes and contents were prepared and tested. Explosion parameters like peak overpressure, impulse, shock energy, and bubble energy were analyzed. It was notable that underwater explosion performance of TiH2/RDX composite explosive was promoted by addition of small particle size TiH2 (D50=0.96 μm), in which case increasing TiH2 content also showed a favorable effect. The maximum increments of specific initial shock energy, bubble energy, and total energy were 10.5%, 6.4%, and 7.1% respectively. However, with bigger TiH2 particle sizes (D50=20.78 μm, D50=136.74 μm), the explosion parameters and the TiH2 content showed a negative relationship, which reveals that TiH2 particle size plays an important role in determining the reactivity of TiH2. Meanwhile, the interaction between TiH2 particle size and content was significant. [ABSTRACT FROM AUTHOR]

The efficacy of thrombolytic therapy for acute ischemic stroke (AIS) decreases when the administration of tissue plasminogen activator (tPA) is delayed. Derived from Toyota Production System, lean production aims to create top-quality products with high-efficiency procedures, a concept that easily applies to emergency medicine. In this study, we aimed to determine whether applying lean principles to flow optimization could hasten the initiation of thrombolysis. A multidisciplinary team (Stroke Team) was organized to implement an ongoing, continuous loop of lean production that contained the following steps: decomposition, recognition, intervention, reengineering and assessment. The door-to-needle time (DNT) and the percentage of patients with DNT ≤ 60 min before and after the adoption of lean principles were used to evaluate the efficiency of our flow optimization. Thirteen patients with AIS in the pre-lean period and 43 patients with AIS in the lean period (23 in lean period I and 20 patients in lean period II) were consecutively enrolled in our study. After flow optimization, we reduced DNT from 90 to 47 min ( p < 0.001). In addition, the percentage of patients treated ≤60 min after hospital arrival increased from 38.46 to 75.0 % ( p = 0.015). Adjusted analysis of covariance confirmed a significant influence of optimization on delay of tPA administration ( p < 0.001). The patients were more likely to have a good prognosis (mRS ≤ 2 at 90 days) after the flow optimization (30.77-75.00 %, p = 0.012). Our study may offer an effective approach for optimizing the thrombolytic flow in the management of AIS. [ABSTRACT FROM AUTHOR]

The hemodynamic alteration in the cerebral circulation caused by the geometric variations in the cerebral circulation arterial network of the circle of Wills (CoW) can lead to fatal ischemic attacks in the brain. The geometric variations due to impairment in the arterial network result in incomplete cerebral arterial structure of CoW and inadequate blood supply to the brain. Therefore, it is of great importance to understand the hemodynamics of the CoW, for efficiently and precisely evaluating the status of blood supply to the brain. In this paper, three-dimensional computational fluid dynamics of the main CoW vasculature coupled with zero-dimensional lumped parameter model boundary condition for the CoW outflow boundaries is developed for analysis of the blood flow distribution in the incomplete CoW cerebral arterial structures. The geometric models in our study cover the arterial segments from the aorta to the cerebral arteries, which can allow us to take into account the innate patient-specific resistance of the arterial trees. Numerical simulations of the governing fluid mechanics are performed to determine the CoW arterial structural hemodynamics, for illustrating the redistribution of the blood flow in CoW due to the structural variations. We have evaluated our coupling methodology in five patient-specific cases that were diagnosed with the absence of efferent vessels or impairment in the connective arteries in their CoWs. The velocity profiles calculated by our approach in the segments of the patient-specific arterial structures are found to be very close to the Doppler ultrasound measurements. The accuracy and consistency of our hemodynamic results have been improved (to $$16.1 \pm 18.5$$ %) compared to that of the pure-resistance boundary conditions (of 43.5 $$\pm $$ 28 %). Based on our grouping of the five cases according to the occurrence of unilateral occlusion in vertebral arteries, the inter-comparison has shown that (i) the flow reduction in posterior cerebral arteries is the consequence of the unilateral vertebral arterial occlusion, and (ii) the flow rate in the anterior cerebral arteries is correlated with the posterior structural variations. This study shows that our coupling approach is capable of providing comprehensive information of the hemodynamic alterations in the pathological CoW arterial structures. The information generated by our methodology can enable evaluation of both the functional and structural status of the clinically significant symptoms, for assisting the treatment decision-making. [ABSTRACT FROM AUTHOR]

Due to a sedentary lifestyle, more and more people are becoming obese nowadays. In addition to health-related problems, obesity can also impair cognition and motor performance. Previous results have shown that obesity mainly affects cognition and motor behaviors through altering brain functions and musculoskeletal system, respectively. Many factors, such as insulin/leptin dysregulation and inflammation, mediate the effect of obesity and cognition and motor behaviors. Substantial evidence has suggested exercise to be an effective way to improve obesity and related cognitive and motor dysfunctions. This paper aims to discuss the association of obesity with cognition and motor behaviors and its underlying mechanisms. Following this, mechanisms of exercise to improve obesity-related dysfunctions are described. Finally, implications and future research direction are raised. [ABSTRACT FROM AUTHOR]

Objectives: Oxygen therapy has been long considered a logical therapy for ischemic stroke. Our previous studies showed that normobaric hyperoxia (normobaric hyperoxia (NBO), 95% O2 with 5% CO2) treatment during ischemia reduced ischemic neuronal death and cerebromicrovascular injury in animal stroke models. In this study, we studied the effects of NBO on the evolution of ischemic brain tissue to infarction in a rat model of transient focal cerebral ischemia. Methods: Male Sprague-Dawley rats were given NBO (95% O2) or normoxia (21% O2) during 90-min filament occlusion of the middle cerebral artery (MCAO), followed by 3 or 22.5 h of reperfusion. 2,3,5-triphenyltetrazolium chloride (TTC) staining was used to evaluate the longitudinal evolution of tissue infarction. Results: In normoxic rats, MCA-supplied cortical and striatal tissue was infarcted after 90-min MCAO with 22.5 h of reperfusion. NBO-treated rats showed a 61.4% reduction in infarct size and tissue infarction mainly occurred in the ischemic striatum. When infarction was assessed at an earlier time point, i.e. at 3 h of reperfusion, normoxic rats showed significantly smaller but mature infarction (no TTC staining, white color), with the infarction mainly occurring in the striatum. Unexpectedly, NBO-treated rats only showed immature lesion (partially stained by TTC, light white color) in the ischemic striatum, indicating that NBO treatment also retarded the process of neuronal death in the ischemic core. Of note, NBO-preserved striatal tissue underwent infarction after prolonged reperfusion. Conclusions: Our results demonstrate that NBO treatment given during cerebral ischemia retards the evolution of ischemic brain tissue toward infarction and NBO-preserved cortical tissue survives better than NBO-preserved striatal tissue during the phase of reperfusion. [ABSTRACT FROM AUTHOR]