Objective: To investigate the changes in CT perfusion between symptomatic and asymptomatic patients with unilateral middle cerebral artery severe stenosis or occlusion.
Methods: A total of 64 consecutive patients with unilateral middle cerebral artery severe stenosis or occlusion admitted to the First Affiliated Hospital of Xinxiang Medical College from January 2019 to March 2022 were retrospectively analyzed and divided into the symptomatic group (n = 33), and the asymptomatic group (n = 31). Clinical data of the two groups were collected. Multivariate logistic regression analysis was performed to analyze the factors of symptomatic and asymptomatic MCA stenosis. A t-test was performed to compare the differences in cerebral perfusion parameters between the two groups.
Results: Multivariate logistic regression analysis indicated that glycosylated hemoglobin levels and high-density lipoprotein cholesterol levels were associated with the development of asymptomatic MCA severe stenosis or occlusion (odds ratio = 1.591 and 0.04, respectively). There were significant differences in CBV, MTT, and TTP between symptomatic and asymptomatic groups (p < 0.05). The CBF of the affected side in the symptomatic group was lower than that of the unaffected side (p < 0.05), whereas the asymptomatic group in CBF was not. Compared with the asymptomatic group, the CBF, MTT, and TTP of the affected side were significantly different (p < 0.05). In contrast, the cerebral perfusion parameters of the unaffected side were not significantly different (p > 0.05).
Conclusion: The use of CT perfusion imaging to analyze the alterations in cerebral perfusion parameters in patients with symptomatic and asymptomatic MCA severe stenosis or occlusion was helpful in clinical diagnosis and selecting treatment strategies and judging the development of the disease.
{"title":"CT Perfusion Alterations in Patients with Symptomatic and Asymptomatic Unilateral Middle Cerebral Artery Severe Stenosis or Occlusion.","authors":"Mengke Ban, Zhigang Zhang, Junyan Yue, Yuhua He, Zhenfang Guo, Ping Zhang","doi":"10.2174/1567202620666230119122237","DOIUrl":"https://doi.org/10.2174/1567202620666230119122237","url":null,"abstract":"<p><strong>Objective: </strong>To investigate the changes in CT perfusion between symptomatic and asymptomatic patients with unilateral middle cerebral artery severe stenosis or occlusion.</p><p><strong>Methods: </strong>A total of 64 consecutive patients with unilateral middle cerebral artery severe stenosis or occlusion admitted to the First Affiliated Hospital of Xinxiang Medical College from January 2019 to March 2022 were retrospectively analyzed and divided into the symptomatic group (n = 33), and the asymptomatic group (n = 31). Clinical data of the two groups were collected. Multivariate logistic regression analysis was performed to analyze the factors of symptomatic and asymptomatic MCA stenosis. A <i>t</i>-test was performed to compare the differences in cerebral perfusion parameters between the two groups.</p><p><strong>Results: </strong>Multivariate logistic regression analysis indicated that glycosylated hemoglobin levels and high-density lipoprotein cholesterol levels were associated with the development of asymptomatic MCA severe stenosis or occlusion (odds ratio = 1.591 and 0.04, respectively). There were significant differences in CBV, MTT, and TTP between symptomatic and asymptomatic groups (<i>p</i> < 0.05). The CBF of the affected side in the symptomatic group was lower than that of the unaffected side (<i>p</i> < 0.05), whereas the asymptomatic group in CBF was not. Compared with the asymptomatic group, the CBF, MTT, and TTP of the affected side were significantly different (<i>p</i> < 0.05). In contrast, the cerebral perfusion parameters of the unaffected side were not significantly different (<i>p</i> > 0.05).</p><p><strong>Conclusion: </strong>The use of CT perfusion imaging to analyze the alterations in cerebral perfusion parameters in patients with symptomatic and asymptomatic MCA severe stenosis or occlusion was helpful in clinical diagnosis and selecting treatment strategies and judging the development of the disease.</p>","PeriodicalId":10879,"journal":{"name":"Current neurovascular research","volume":"20 1","pages":"62-69"},"PeriodicalIF":2.1,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9745895","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-04-14DOI: 10.2174/1567202619666220414093130
Yuan Chen, Miaomiao Chi, Xinyue Qiao, Jiabing Wang, Yong Jin
BACKGROUND Sepsis frequently occurs in patients after infection and is highly associated with death. Septic encephalopathy is characterized by dysfunction of the central nervous system, of which the root cause is a systemic inflammatory response. Sepsis-associated encephalopathy is a severe disease that frequently occurs in children, resulting in high morbidity and mortality. OBJECTIVES In the present study, we aim to investigate the neuroprotective mechanism of ginsenoside Rg1 in response to septic encephalopathy. METHODS Effects of ginsenoside Rg1 on septic encephalopathy were determined by cell viability, cytotoxicity, ROS responses, and apoptosis assays and histological examination of brain. Inflammatory activities were evaluated by expression levels of IL-1β, IL-6, IL-10, TNF-α, and MCP-1 using qPCR and ELISA. Activities of signaling pathways in inflammation were estimated by the production of p-Erk1/2/Erk1/2, p-JNK/JNK, p-p38/p38, p-p65/p65, and p-IkBα/IkBα using western blot. RESULTS LPS simulation resulted in a significant increase in cytotoxicity, ROS responses, and apoptosis and a significant decrease in cell viability in CTX TNA2 cells, as well as brain damage in rats. Moreover, the production of IL-1β, IL-6, IL-10, TNF-α, and MCP-1 was significantly stimulated both in CTX TNA2 cells and in the brain, which confirmed the establishment of vitro and in vivo models of septic encephalopathy. The damage and inflammatory responses induced by LPS were significantly decreased by treatment with Rg1. Western blot analyses indicated Rg1 significantly decreased the production of p-Erk1/2/Erk1/2, p-JNK/JNK, p-p38/p38, p-p65/p65, and p-IkBα/IkBα in LPS-induced CTX TNA2 cells and in the brain. CONCLUSIONS These findings suggested that Rg1 inhibited the activation of NF-κB and MAPK signaling pathways, which activate the production of proinflammatory cytokines and chemokines. The findings of this study suggest that ginsenoside Rg1 is a candidate treatment for septic encephalopathy.
{"title":"Anti-inflammatory effect of ginsenoside Rg1 on LPS-induced septic encephalopathy and associated mechanism.","authors":"Yuan Chen, Miaomiao Chi, Xinyue Qiao, Jiabing Wang, Yong Jin","doi":"10.2174/1567202619666220414093130","DOIUrl":"https://doi.org/10.2174/1567202619666220414093130","url":null,"abstract":"BACKGROUND\u0000Sepsis frequently occurs in patients after infection and is highly associated with death. Septic encephalopathy is characterized by dysfunction of the central nervous system, of which the root cause is a systemic inflammatory response. Sepsis-associated encephalopathy is a severe disease that frequently occurs in children, resulting in high morbidity and mortality.\u0000\u0000\u0000OBJECTIVES\u0000In the present study, we aim to investigate the neuroprotective mechanism of ginsenoside Rg1 in response to septic encephalopathy.\u0000\u0000\u0000METHODS\u0000Effects of ginsenoside Rg1 on septic encephalopathy were determined by cell viability, cytotoxicity, ROS responses, and apoptosis assays and histological examination of brain. Inflammatory activities were evaluated by expression levels of IL-1β, IL-6, IL-10, TNF-α, and MCP-1 using qPCR and ELISA. Activities of signaling pathways in inflammation were estimated by the production of p-Erk1/2/Erk1/2, p-JNK/JNK, p-p38/p38, p-p65/p65, and p-IkBα/IkBα using western blot.\u0000\u0000\u0000RESULTS\u0000LPS simulation resulted in a significant increase in cytotoxicity, ROS responses, and apoptosis and a significant decrease in cell viability in CTX TNA2 cells, as well as brain damage in rats. Moreover, the production of IL-1β, IL-6, IL-10, TNF-α, and MCP-1 was significantly stimulated both in CTX TNA2 cells and in the brain, which confirmed the establishment of vitro and in vivo models of septic encephalopathy. The damage and inflammatory responses induced by LPS were significantly decreased by treatment with Rg1. Western blot analyses indicated Rg1 significantly decreased the production of p-Erk1/2/Erk1/2, p-JNK/JNK, p-p38/p38, p-p65/p65, and p-IkBα/IkBα in LPS-induced CTX TNA2 cells and in the brain.\u0000\u0000\u0000CONCLUSIONS\u0000These findings suggested that Rg1 inhibited the activation of NF-κB and MAPK signaling pathways, which activate the production of proinflammatory cytokines and chemokines. The findings of this study suggest that ginsenoside Rg1 is a candidate treatment for septic encephalopathy.","PeriodicalId":10879,"journal":{"name":"Current neurovascular research","volume":"1 1","pages":""},"PeriodicalIF":2.1,"publicationDate":"2022-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41425431","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-04-06DOI: 10.2174/1567202619666220406084947
Zhaoxian Yan, Xin Zhang, Lin Hua, Lifa Huang
OBJECTIVES Melatonin (MT) is a pineal hormone with antineoplastic potential. This study aims to explore the therapeutic potential and mechanism of MT on glioblastoma (GBM). METHODS A human GBM cell line, LN229 was used for evaluating the function of MT. Cell viability, apoptosis, and migration were detected by CCK-8, flow cytometry, and transwell assays, respectively. The mRNA and protein expression of specific genes were measured by qRT-PCR and western blot, respectively. The regulatory relationship between miR-16-5p and PIM1 was validated by dual luciferase reporter gene assay. A mouse xenograft model was established to prove the anti-tumor effect and related mechanisms of MT in vivo. RESULTS MT inhibited the viability and migration, and promoted the apoptosis of LN229 cells in a dose-dependent manner. MiR-16-5p was dose-dependently up-regulated by MT in LN229 cells, which negatively regulated its target PIM1. MiR-16-5p inhibitor eliminated the anti-tumor effect of MT in LN229 cells, while si-PIM1 reversed the effect of miR-16-5p inhibitor in MT-treated cells. MT inhibited the tumor growth in vivo and MT-induced PIM1 down-regulation was reversed by miR-16-5p inhibition in tumor tissues. CONCLUSIONS MT inhibits the malignant progression of GBM via regulating miR-16-5p-midiated PIM1.
{"title":"Melatonin inhibits the malignant progression of glioblastoma via regulating miR-16-5p/PIM1.","authors":"Zhaoxian Yan, Xin Zhang, Lin Hua, Lifa Huang","doi":"10.2174/1567202619666220406084947","DOIUrl":"https://doi.org/10.2174/1567202619666220406084947","url":null,"abstract":"OBJECTIVES\u0000Melatonin (MT) is a pineal hormone with antineoplastic potential. This study aims to explore the therapeutic potential and mechanism of MT on glioblastoma (GBM).\u0000\u0000\u0000METHODS\u0000A human GBM cell line, LN229 was used for evaluating the function of MT. Cell viability, apoptosis, and migration were detected by CCK-8, flow cytometry, and transwell assays, respectively. The mRNA and protein expression of specific genes were measured by qRT-PCR and western blot, respectively. The regulatory relationship between miR-16-5p and PIM1 was validated by dual luciferase reporter gene assay. A mouse xenograft model was established to prove the anti-tumor effect and related mechanisms of MT in vivo.\u0000\u0000\u0000RESULTS\u0000MT inhibited the viability and migration, and promoted the apoptosis of LN229 cells in a dose-dependent manner. MiR-16-5p was dose-dependently up-regulated by MT in LN229 cells, which negatively regulated its target PIM1. MiR-16-5p inhibitor eliminated the anti-tumor effect of MT in LN229 cells, while si-PIM1 reversed the effect of miR-16-5p inhibitor in MT-treated cells. MT inhibited the tumor growth in vivo and MT-induced PIM1 down-regulation was reversed by miR-16-5p inhibition in tumor tissues.\u0000\u0000\u0000CONCLUSIONS\u0000MT inhibits the malignant progression of GBM via regulating miR-16-5p-midiated PIM1.","PeriodicalId":10879,"journal":{"name":"Current neurovascular research","volume":" ","pages":""},"PeriodicalIF":2.1,"publicationDate":"2022-04-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42192082","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-04-06DOI: 10.2174/1567202619666220406102429
Yuan Yang, Ting Cui, Xueling Bai, Anmo Wang, Xuening Zhang, Jincheng Wan, Changyi Wang, Kun Lu, Fayun Hu, Bo Wu
BACKGROUND/OBJECTIVE Systemic immune-inflammation index (SII) is a novel inflammatory factor, which may be involved in the destruction of the blood-brain barrier (BBB) after acute ischemic stroke (AIS); however, the association between SII and symptomatic intracranial hemorrhage (sICH) in AIS patients undergoing endovascular treatment (EVT) remains unclear. METHODS Patients with acute ischemic stroke due to large vessel occlusion (AIS-LVO) who underwent EVT were consecutively enrolled. Blood samples were collected in the emergency room and SII was calculated by neutrophils × platelets/lymphocytes. Participants were categorized into tertiles according to admission SII. The main outcome was defined as the occurrence of sICH, following the European Cooperative Acute Stroke Study III (ECASS-III) criteria. RESULTS A total of 379 AIS-LVO patients with EVT were enrolled (median age = 71 years, 52.5% males). The median baseline National Institutes of Health Stroke Scale (NIHSS) score was 15 (IQR, 12-18). The median of SII was 820.9 × 109/L (IQR, 473.1-1345.2). Forty-three (11.3%) patients who developed sICH. SII was found to be independently associated with sICH after EVT (adjusted odd ratio (OR) = 1.005 (per 10 units increase); 95% confidence interval (CI): 1.002-1.008; p = 0.002). Compared to patients in the lowest SII tertile, patients in the highest tertile had a higher risk of sICH (adj-OR 3.379; 95% CI 1.302-8.768; p = 0.012). The risk of sICH increased with the increase of SII in a dose-dependent manner (p for trend = 0.004). There was no interaction between potential modifiers and SII on sICH. CONCLUSIONS Admission SII positively associated with sICH in AIS-LVO patients treated with EVT. These results need to be confirmed in future studies.
背景/目的系统免疫炎症指数（SII）是一种新的炎症因子，可能参与急性缺血性脑卒中（AIS）后血脑屏障（BBB）的破坏；然而，在接受血管内治疗（EVT）的AIS患者中，SII与症状性颅内出血（sICH）之间的关系尚不清楚。方法对接受EVT的大血管闭塞性急性缺血性脑卒中（AIS-LVO）患者进行连续入组。在急诊室采集血样，通过中性粒细胞×血小板/淋巴细胞计算SII。参与者根据入院SII分为三组。根据欧洲合作急性卒中研究III（ECASS-III）标准，主要结果被定义为sICH的发生。结果共纳入379名患有EVT的AIS-LVO患者（中位年龄=71岁，52.5%为男性）。美国国立卫生研究院卒中量表（NIHSS）的中位基线评分为15（IQR，12-18）。SII的中位数为820.9×109/L（IQR，473.1-1345.2）。43名（11.3%）患者出现了sICH。研究发现，EVT后SII与sICH独立相关（调整后的奇数比（OR）=1.005（每增加10个单位）；95%置信区间（CI）：1.002-1.008；p=0.002）。与SII最低三分位数的患者相比，SII最高三分位数患者的sICH风险更高（adj OR 3.379；95%CI 1.302-8.768；p=0.012）。sICH的风险随着SII的增加而增加，呈剂量依赖性（趋势p=0.004）。潜在修饰物和SII对sICH没有相互作用。结论EVT治疗的AIS-LVO患者的入院SII与sICH呈正相关。这些结果需要在未来的研究中得到证实。
{"title":"Association between Systemic Immune-Inflammation Index and Symptomatic Intracranial Hemorrhage in Acute Ischemic Stroke Patients Undergoing Endovascular Treatment.","authors":"Yuan Yang, Ting Cui, Xueling Bai, Anmo Wang, Xuening Zhang, Jincheng Wan, Changyi Wang, Kun Lu, Fayun Hu, Bo Wu","doi":"10.2174/1567202619666220406102429","DOIUrl":"https://doi.org/10.2174/1567202619666220406102429","url":null,"abstract":"BACKGROUND/OBJECTIVE\u0000Systemic immune-inflammation index (SII) is a novel inflammatory factor, which may be involved in the destruction of the blood-brain barrier (BBB) after acute ischemic stroke (AIS); however, the association between SII and symptomatic intracranial hemorrhage (sICH) in AIS patients undergoing endovascular treatment (EVT) remains unclear.\u0000\u0000\u0000METHODS\u0000Patients with acute ischemic stroke due to large vessel occlusion (AIS-LVO) who underwent EVT were consecutively enrolled. Blood samples were collected in the emergency room and SII was calculated by neutrophils × platelets/lymphocytes. Participants were categorized into tertiles according to admission SII. The main outcome was defined as the occurrence of sICH, following the European Cooperative Acute Stroke Study III (ECASS-III) criteria.\u0000\u0000\u0000RESULTS\u0000A total of 379 AIS-LVO patients with EVT were enrolled (median age = 71 years, 52.5% males). The median baseline National Institutes of Health Stroke Scale (NIHSS) score was 15 (IQR, 12-18). The median of SII was 820.9 × 109/L (IQR, 473.1-1345.2). Forty-three (11.3%) patients who developed sICH. SII was found to be independently associated with sICH after EVT (adjusted odd ratio (OR) = 1.005 (per 10 units increase); 95% confidence interval (CI): 1.002-1.008; p = 0.002). Compared to patients in the lowest SII tertile, patients in the highest tertile had a higher risk of sICH (adj-OR 3.379; 95% CI 1.302-8.768; p = 0.012). The risk of sICH increased with the increase of SII in a dose-dependent manner (p for trend = 0.004). There was no interaction between potential modifiers and SII on sICH.\u0000\u0000\u0000CONCLUSIONS\u0000Admission SII positively associated with sICH in AIS-LVO patients treated with EVT. These results need to be confirmed in future studies.","PeriodicalId":10879,"journal":{"name":"Current neurovascular research","volume":" ","pages":""},"PeriodicalIF":2.1,"publicationDate":"2022-04-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48091951","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-04-06DOI: 10.2174/1567202619666220406100320
Y. Xi, Yafei Chi, Jing Han, Hong-R Li, Xianyun Wang, Xuan Wang, Tiantian Li, Hui-yan Yu, Rong Xiao
BACKGROUND β-amyloid peptides (Aβ) induced oxidative damage contributes to the pathogenesis of neurodegenerative diseases and cerebrovascular system is more vulnerable to oxidative stress. Our earlier study showed a clue that Genistein (Gen) might activate Nf-E2 related factor 2 (Nrf2) pathway to protect cerebrovascular cells from oxidative damage induced by Aβ, but the specific mechanisms and regulation targets are unclear. OBJECTIVE In this study, the anti-oxidative effects and the possible targets of Gen on regulating Nrf2 pathway in bEnd.3 cells were investigated. Cells were divided into control, Aβ25-35, Gen and Gen+Aβ25-35 groups. METHODS Cell viability, levels of malondialdehyde (MDA), Superoxide Dismutase (SOD) activity and nitrotyrosine were evaluated. Moreover, mRNA and/or protein expressions of Nrf2 and kelch-like ECH-associated protein 1 (Keap1) were measured. Then we transfected Keap1 over-expressed plasmid into bEnd.3 cells and measured the protein expressions of Nrf2 pathway related factors. Data showed that Gen could inhibit the over-production of MDA and nitrotyrosine and activate SOD activity. Besides we got the phenomenon that Gen could up-regulate the mRNA and protein expressions of Nrf2 and down-regulate Keap1 protein expression, the Keap1 over-expressed plasmid study indicated that the up-regulation of Nrf2 protein expression induced by pretreatment of Gen could be blocked by the transfection of Keap1 over-expressed plasmid, and the same results also occurred in Nrf2 downstream factors. CONCLUSION Gen could alleviate the cerebrovascular cells oxidative damage induced by Aβ25-35 through regulating Nrf2 pathway, and Keap1 might be one of the targets of Gen on activating Nrf2 pathway.
{"title":"Keap1 as Target of Genistein on Nrf2 Signaling Pathway Antagonizing Aβ induced Oxidative Damage of Cerebrovascular Endothelial Cells.","authors":"Y. Xi, Yafei Chi, Jing Han, Hong-R Li, Xianyun Wang, Xuan Wang, Tiantian Li, Hui-yan Yu, Rong Xiao","doi":"10.2174/1567202619666220406100320","DOIUrl":"https://doi.org/10.2174/1567202619666220406100320","url":null,"abstract":"BACKGROUND\u0000β-amyloid peptides (Aβ) induced oxidative damage contributes to the pathogenesis of neurodegenerative diseases and cerebrovascular system is more vulnerable to oxidative stress. Our earlier study showed a clue that Genistein (Gen) might activate Nf-E2 related factor 2 (Nrf2) pathway to protect cerebrovascular cells from oxidative damage induced by Aβ, but the specific mechanisms and regulation targets are unclear.\u0000\u0000\u0000OBJECTIVE\u0000In this study, the anti-oxidative effects and the possible targets of Gen on regulating Nrf2 pathway in bEnd.3 cells were investigated. Cells were divided into control, Aβ25-35, Gen and Gen+Aβ25-35 groups.\u0000\u0000\u0000METHODS\u0000Cell viability, levels of malondialdehyde (MDA), Superoxide Dismutase (SOD) activity and nitrotyrosine were evaluated. Moreover, mRNA and/or protein expressions of Nrf2 and kelch-like ECH-associated protein 1 (Keap1) were measured. Then we transfected Keap1 over-expressed plasmid into bEnd.3 cells and measured the protein expressions of Nrf2 pathway related factors. Data showed that Gen could inhibit the over-production of MDA and nitrotyrosine and activate SOD activity. Besides we got the phenomenon that Gen could up-regulate the mRNA and protein expressions of Nrf2 and down-regulate Keap1 protein expression, the Keap1 over-expressed plasmid study indicated that the up-regulation of Nrf2 protein expression induced by pretreatment of Gen could be blocked by the transfection of Keap1 over-expressed plasmid, and the same results also occurred in Nrf2 downstream factors.\u0000\u0000\u0000CONCLUSION\u0000Gen could alleviate the cerebrovascular cells oxidative damage induced by Aβ25-35 through regulating Nrf2 pathway, and Keap1 might be one of the targets of Gen on activating Nrf2 pathway.","PeriodicalId":10879,"journal":{"name":"Current neurovascular research","volume":"3 1","pages":""},"PeriodicalIF":2.1,"publicationDate":"2022-04-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"67876304","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-04-06DOI: 10.2174/1567202619666220406082221
Kelu Li, Ping-ping Ning, Bin Liu, Hongju Yang, Yongyun Zhu, Weifang Yin, Chuanbin Zhou, Hui Ren, Xinglong Yang
BACKGROUND Parkinson's disease (PD) is associated with coiled-coil-helix-coiled-coil-helix domain containing 2 (CHCHD2) downregulation, which has been linked to reduced cyclocytase activity and increased levels of oxygen free radicals, leading to mitochondrial fragmentation and apoptosis. Little is known about how CHCHD2 normally functions in the cell and, therefore, how its downregulation may contribute to PD. OBJECTIVE This study aimed to identify such target genes using chromatin immunoprecipitation sequencing from SH-SY5Y human neuroblastoma cells treated with neurotoxin 1-methyl-4-phenylpyridinium (MPP+) as a PD model. METHODS In this study, we established a MPP+ -reated SH-SY5Y cell model and evaluated the effects of CHCHD2 overexpression on cell proliferation and apoptosis. At the same time, we used high-throughput chromatin immunoprecipitation sequencing to identify its downstream target gene in SH-SY5Y cells. In addition, we verified the possible downstream target genes and discussed their mechanisms. RESULTS The expression level of α-synuclein increased in SH-SY5Y cells treated with MPP+, while the protein expression level of CHCHD2 decreased significantly, especially after 24 h of treatment. Chip-IP results showed that CHCHD2 may regulate potential target genes such as HDX, ACP1, RAVER2, C1orf229, RN7SL130, GNPTG, erythroid 2 Like 2 (NFE2L2), required for cell differentiation 1 homologue (RQCD1), solute carrier family 5 member 7 (SLA5A7), and N-Acetyltransferase 8 Like (NAT8L). NFE2L2 and RQCD1 were validated as targets using PCR and western blotting of immunoprecipitates, and these two genes together with SLA5A7 and NAT8L were upregulated in SH-SY5Y cells overexpressing CHCHD2. Downregulation of CHCHD2 may contribute to PD by leading to inadequate expression of NFE2L2 and RQCD1 as well as, potentially, SLA5A7 and NAT8L. CONCLUSION Our results suggest that CHCHD2 plays a protective role by maintaining mitochondrial homeostasis and promoting proliferation in neurons. In this study, the changes of CHCHD2 and downstream target genes such as NFE2L2/RQCD1 may have potential application prospects in the future. These findings provide leads to explore PD pathogenesis and potential treatments.
背景:帕金森病(PD)与含2螺旋结构域(CHCHD2)下调有关，这与环切酶活性降低和氧自由基水平升高有关，导致线粒体断裂和凋亡。关于CHCHD2在细胞中的正常功能以及其下调如何导致PD，我们知之甚少。目的利用神经毒素1-甲基-4-苯基吡啶(MPP+)处理的SH-SY5Y人神经母细胞瘤细胞的染色质免疫沉淀测序，鉴定PD模型中的靶基因。方法建立MPP+诱导SH-SY5Y细胞模型，观察CHCHD2过表达对SH-SY5Y细胞增殖和凋亡的影响。同时，我们利用高通量染色质免疫沉淀测序鉴定其在SH-SY5Y细胞中的下游靶基因。此外，我们还验证了可能的下游靶基因，并讨论了它们的作用机制。结果经MPP+处理的SH-SY5Y细胞α-synuclein表达水平升高，而CHCHD2蛋白表达水平明显降低，尤其是处理24 h后。Chip-IP结果显示，CHCHD2可能调控HDX、ACP1、RAVER2、C1orf229、RN7SL130、GNPTG、红细胞2 Like 2 (NFE2L2)、细胞分化1同源物(RQCD1)、溶质载体家族5成员7 (SLA5A7)和n -乙酰转移酶8 Like (NAT8L)等潜在靶基因。通过PCR和免疫沉淀的western blotting验证了NFE2L2和RQCD1是靶点，这两个基因与SLA5A7和NAT8L在过表达CHCHD2的SH-SY5Y细胞中表达上调。CHCHD2的下调可能通过导致NFE2L2和RQCD1以及潜在的SLA5A7和NAT8L的表达不足而导致PD。结论CHCHD2通过维持线粒体稳态和促进神经元增殖发挥保护作用。在本研究中，CHCHD2及下游靶基因如NFE2L2/RQCD1的变化在未来可能具有潜在的应用前景。这些发现为探索帕金森病的发病机制和潜在的治疗提供了线索。
{"title":"Downregulation of CHCHD2 may Contribute to Parkinson's Disease by Reducing Expression of NFE2L2 and RQCD1.","authors":"Kelu Li, Ping-ping Ning, Bin Liu, Hongju Yang, Yongyun Zhu, Weifang Yin, Chuanbin Zhou, Hui Ren, Xinglong Yang","doi":"10.2174/1567202619666220406082221","DOIUrl":"https://doi.org/10.2174/1567202619666220406082221","url":null,"abstract":"BACKGROUND\u0000Parkinson's disease (PD) is associated with coiled-coil-helix-coiled-coil-helix domain containing 2 (CHCHD2) downregulation, which has been linked to reduced cyclocytase activity and increased levels of oxygen free radicals, leading to mitochondrial fragmentation and apoptosis. Little is known about how CHCHD2 normally functions in the cell and, therefore, how its downregulation may contribute to PD.\u0000\u0000\u0000OBJECTIVE\u0000This study aimed to identify such target genes using chromatin immunoprecipitation sequencing from SH-SY5Y human neuroblastoma cells treated with neurotoxin 1-methyl-4-phenylpyridinium (MPP+) as a PD model.\u0000\u0000\u0000METHODS\u0000In this study, we established a MPP+ -reated SH-SY5Y cell model and evaluated the effects of CHCHD2 overexpression on cell proliferation and apoptosis. At the same time, we used high-throughput chromatin immunoprecipitation sequencing to identify its downstream target gene in SH-SY5Y cells. In addition, we verified the possible downstream target genes and discussed their mechanisms.\u0000\u0000\u0000RESULTS\u0000The expression level of α-synuclein increased in SH-SY5Y cells treated with MPP+, while the protein expression level of CHCHD2 decreased significantly, especially after 24 h of treatment. Chip-IP results showed that CHCHD2 may regulate potential target genes such as HDX, ACP1, RAVER2, C1orf229, RN7SL130, GNPTG, erythroid 2 Like 2 (NFE2L2), required for cell differentiation 1 homologue (RQCD1), solute carrier family 5 member 7 (SLA5A7), and N-Acetyltransferase 8 Like (NAT8L). NFE2L2 and RQCD1 were validated as targets using PCR and western blotting of immunoprecipitates, and these two genes together with SLA5A7 and NAT8L were upregulated in SH-SY5Y cells overexpressing CHCHD2. Downregulation of CHCHD2 may contribute to PD by leading to inadequate expression of NFE2L2 and RQCD1 as well as, potentially, SLA5A7 and NAT8L.\u0000\u0000\u0000CONCLUSION\u0000Our results suggest that CHCHD2 plays a protective role by maintaining mitochondrial homeostasis and promoting proliferation in neurons. In this study, the changes of CHCHD2 and downstream target genes such as NFE2L2/RQCD1 may have potential application prospects in the future. These findings provide leads to explore PD pathogenesis and potential treatments.","PeriodicalId":10879,"journal":{"name":"Current neurovascular research","volume":" ","pages":""},"PeriodicalIF":2.1,"publicationDate":"2022-04-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47111705","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-04-06DOI: 10.2174/1567202619666220406092532
Jincheng Wan, W. Kwapong, W. Tao, Kun Lu, Shuai Jiang, Hongbo Zheng, Fayun Hu, Bo Wu
BACKGROUND Carotid artery stenosis (CAS) patients show reduced blood flow in the ophthalmic artery. This study aimed to assess the changes in the choriocapillaris and choroidal thickness in patients with unilateral carotid artery stenosis after carotid stenting using swept-source optical coherence tomography (SS-OCT)/swept-source optical coherence tomography angiography (SS-OCTA). METHODS Fifty-three mild to moderate CAS patients and 40 controls were enrolled in this study. All participants underwent digital subtraction angiography (DSA) and SS-OCT/SS-OCTAA imaging before and 4 days after carotid artery stenting. SS-OCTA was used to image and measure the perfusion of the choriocapillaris (mm2) while SS-OCT was used to image and measure the choroidal thickness (µm). The stenosed side was described as the ipsilateral eye while the other side was the contralateral eye. RESULTS Choroidal thickness was significantly thinner (P = 0.024) in CAS when compared with controls. Ipsilateral eyes of CAS patients showed significantly thinner (P = 0.008) choroidal thickness when compared with contralateral eyes. Ipsilateral eyes of CAS patients showed thicker (P = 0.027) choroidal thickness after carotid artery stenting while contralateral eyes showed thinner choroidal thickness (P = 0.039). CONCLUSIONS Our report suggests that in vivo quantification of the choroid with the SS-OCT/SS-OCTA may allow monitoring of CAS and enable the assessment of purported treatments.
{"title":"Choroidal changes in carotid stenosis patients after stenting detected by swept-source optical coherence tomography angiography.","authors":"Jincheng Wan, W. Kwapong, W. Tao, Kun Lu, Shuai Jiang, Hongbo Zheng, Fayun Hu, Bo Wu","doi":"10.2174/1567202619666220406092532","DOIUrl":"https://doi.org/10.2174/1567202619666220406092532","url":null,"abstract":"BACKGROUND\u0000Carotid artery stenosis (CAS) patients show reduced blood flow in the ophthalmic artery. This study aimed to assess the changes in the choriocapillaris and choroidal thickness in patients with unilateral carotid artery stenosis after carotid stenting using swept-source optical coherence tomography (SS-OCT)/swept-source optical coherence tomography angiography (SS-OCTA).\u0000\u0000\u0000METHODS\u0000Fifty-three mild to moderate CAS patients and 40 controls were enrolled in this study. All participants underwent digital subtraction angiography (DSA) and SS-OCT/SS-OCTAA imaging before and 4 days after carotid artery stenting. SS-OCTA was used to image and measure the perfusion of the choriocapillaris (mm2) while SS-OCT was used to image and measure the choroidal thickness (µm). The stenosed side was described as the ipsilateral eye while the other side was the contralateral eye.\u0000\u0000\u0000RESULTS\u0000Choroidal thickness was significantly thinner (P = 0.024) in CAS when compared with controls. Ipsilateral eyes of CAS patients showed significantly thinner (P = 0.008) choroidal thickness when compared with contralateral eyes. Ipsilateral eyes of CAS patients showed thicker (P = 0.027) choroidal thickness after carotid artery stenting while contralateral eyes showed thinner choroidal thickness (P = 0.039).\u0000\u0000\u0000CONCLUSIONS\u0000Our report suggests that in vivo quantification of the choroid with the SS-OCT/SS-OCTA may allow monitoring of CAS and enable the assessment of purported treatments.","PeriodicalId":10879,"journal":{"name":"Current neurovascular research","volume":" ","pages":""},"PeriodicalIF":2.1,"publicationDate":"2022-04-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42558381","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-03-16DOI: 10.2174/1567202619666220316112509
Fan Zhang, Zhi-Hua Wang, Bei Sun, Yan-kun Huang, Cheng Chen, Jie Hu, Longyan Li, Ping-ping Xia, Z. Ye
OBJECTIVE Evidences had demonstrated that propofol attenuated neuro-inflammation following brain ischemia. Moreover, LncRNA-MEG3 was identified as an independent prognostic marker for ischemic stroke patients, and was found to be correlated with cerebral ischemia in animal models. Therefore, the current study explored the role of propofol on lipopolysaccharide (LPS)-mediated inflammation in cultured astrocytes, along with the molecular mechanism involved in LncRNA-MEG3/NF-κB axis. METHODS The primary cultured astrocytes isolated from rats were used to establish an inflammatory model, which were treated with LPS. Propofol was administrated to the primary cultured astrocytes during LPS treatment. The effect of propofol on pro-inflammatory cytokines and the LncRNA-MEG3/NF-κB pathway were detected by ELISA, qRT-PCR and Western Blot assay, respectively. Then, dual-luciferase assay, chromatin immunoprecipitation and RNA immunoprecipitation were used to determine the interaction between LncRNA-MEG3 and NF-κB. RESULTS Our study found that propofol significantly reduced LncRNA-MEG3 expression, which was elevated in LPS-stimulated astrocytes. Moreover, both propofol and LncRNA-MEG3 knockdown remarkably alleviated LPS-induced cytotoxicity by suppressing expressions and release of pro-inflammatory cytokines. Loss of LncRNA-MEG3 notably suppressed the NF-κB activity and its phosphorylated activation. Additionally, it was also observed that LncRNA-MEG3 could bind nuclear p65/p50, and promote the binding of NF-κB to IL-6 and TNF-α promoters in the nucleus, subsequently stimulating the production of inflammatory cytokines in LPS-treated astrocytes. Furthermore, a specific inhibitor of NF-κB, PDTC rescued astrocytes from LPS exposure without affecting LncRNA-MEG3 expression. CONCLUSION These findings demonstrated that LncRNA-MEG3 acted as a positive regulator of NF-κB, mediated the neuroprotection of propofol in LPS-triggered astrocytes injury.
{"title":"Propofol rescued astrocytes from LPS-induced inflammatory response via blocking LncRNA-MEG3/NF-κB axis.","authors":"Fan Zhang, Zhi-Hua Wang, Bei Sun, Yan-kun Huang, Cheng Chen, Jie Hu, Longyan Li, Ping-ping Xia, Z. Ye","doi":"10.2174/1567202619666220316112509","DOIUrl":"https://doi.org/10.2174/1567202619666220316112509","url":null,"abstract":"OBJECTIVE\u0000Evidences had demonstrated that propofol attenuated neuro-inflammation following brain ischemia. Moreover, LncRNA-MEG3 was identified as an independent prognostic marker for ischemic stroke patients, and was found to be correlated with cerebral ischemia in animal models. Therefore, the current study explored the role of propofol on lipopolysaccharide (LPS)-mediated inflammation in cultured astrocytes, along with the molecular mechanism involved in LncRNA-MEG3/NF-κB axis.\u0000\u0000\u0000METHODS\u0000The primary cultured astrocytes isolated from rats were used to establish an inflammatory model, which were treated with LPS. Propofol was administrated to the primary cultured astrocytes during LPS treatment. The effect of propofol on pro-inflammatory cytokines and the LncRNA-MEG3/NF-κB pathway were detected by ELISA, qRT-PCR and Western Blot assay, respectively. Then, dual-luciferase assay, chromatin immunoprecipitation and RNA immunoprecipitation were used to determine the interaction between LncRNA-MEG3 and NF-κB.\u0000\u0000\u0000RESULTS\u0000Our study found that propofol significantly reduced LncRNA-MEG3 expression, which was elevated in LPS-stimulated astrocytes. Moreover, both propofol and LncRNA-MEG3 knockdown remarkably alleviated LPS-induced cytotoxicity by suppressing expressions and release of pro-inflammatory cytokines. Loss of LncRNA-MEG3 notably suppressed the NF-κB activity and its phosphorylated activation. Additionally, it was also observed that LncRNA-MEG3 could bind nuclear p65/p50, and promote the binding of NF-κB to IL-6 and TNF-α promoters in the nucleus, subsequently stimulating the production of inflammatory cytokines in LPS-treated astrocytes. Furthermore, a specific inhibitor of NF-κB, PDTC rescued astrocytes from LPS exposure without affecting LncRNA-MEG3 expression.\u0000\u0000\u0000CONCLUSION\u0000These findings demonstrated that LncRNA-MEG3 acted as a positive regulator of NF-κB, mediated the neuroprotection of propofol in LPS-triggered astrocytes injury.","PeriodicalId":10879,"journal":{"name":"Current neurovascular research","volume":" ","pages":""},"PeriodicalIF":2.1,"publicationDate":"2022-03-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43050121","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
BACKGROUND MicroRNAs (miRNAs) may participate in the process of vascular calcification. However, the role of microRNA-17-5p in vascular calcification has not been clarified. In this study, we showed the effects of microRNA-17-5p on vascular calcification. MATERIALS AND METHODS Vascular smooth muscle cells (VSMCs) were transfected with miR-17-5p mimics, an miR-17-5p inhibitor or a negative control (NC) using Lipofectamine 2000. Then the cells were induced by an osteogenic medium. Alkaline phosphatase (ALP) activity and mineralization were determined. Osteocalcin (OC), bone morphogenetic protein 2(BMP-2), Col1agren Ia (Colla), Runx2 and ankylosis protein homolog (ANKH) gene expressions were determined by reverse transcription-polymerase chain reaction. Vascular calcification was developed using a renal failure model. RESULTS The ALP activity was increased when miR-17-5p mimics were transfected, whereas the miR-17-5p inhibitor reduced ALP activity (p < 0.05). The number and average area of mineral node in miR-17-5p mimics group were larger than those in corresponding control and NC groups (p < 0.05). The number and average area of the mineral nodes in the miR-17-5p inhibitor group were smaller than those in corresponding control and NC groups (p < 0.05). Bmp2, OC, Col1a and Runx2 were higher in the miR-17-5p mimics group compared to those in the control and NC groups. ANKH expression was decreased in VSMCs with the miR-17-5p mimics and increased in VSMCs with miR-17-5p inhibitor. ANKH siRNA intervention also promoted mineralization. The miR-17-5p expression was upregulated and ANKH was down-regulated in the aortic arteries with calcification. CONCLUSION Our data showed that miR-17-5p may promote vascular calcification by inhibiting ANKH expression.
{"title":"MicroRNA-17-5p promotes vascular calcification by targeting ANKH.","authors":"Chao Shi, Jiaorong Tan, Jian-can Lu, Junling Huang, Xiangqi Li, Jiahong Xu, Xing Wang","doi":"10.2174/1567202619666220316115425","DOIUrl":"https://doi.org/10.2174/1567202619666220316115425","url":null,"abstract":"BACKGROUND\u0000MicroRNAs (miRNAs) may participate in the process of vascular calcification. However, the role of microRNA-17-5p in vascular calcification has not been clarified. In this study, we showed the effects of microRNA-17-5p on vascular calcification.\u0000\u0000\u0000MATERIALS AND METHODS\u0000Vascular smooth muscle cells (VSMCs) were transfected with miR-17-5p mimics, an miR-17-5p inhibitor or a negative control (NC) using Lipofectamine 2000. Then the cells were induced by an osteogenic medium. Alkaline phosphatase (ALP) activity and mineralization were determined. Osteocalcin (OC), bone morphogenetic protein 2(BMP-2), Col1agren Ia (Colla), Runx2 and ankylosis protein homolog (ANKH) gene expressions were determined by reverse transcription-polymerase chain reaction. Vascular calcification was developed using a renal failure model.\u0000\u0000\u0000RESULTS\u0000The ALP activity was increased when miR-17-5p mimics were transfected, whereas the miR-17-5p inhibitor reduced ALP activity (p < 0.05). The number and average area of mineral node in miR-17-5p mimics group were larger than those in corresponding control and NC groups (p < 0.05). The number and average area of the mineral nodes in the miR-17-5p inhibitor group were smaller than those in corresponding control and NC groups (p < 0.05). Bmp2, OC, Col1a and Runx2 were higher in the miR-17-5p mimics group compared to those in the control and NC groups. ANKH expression was decreased in VSMCs with the miR-17-5p mimics and increased in VSMCs with miR-17-5p inhibitor. ANKH siRNA intervention also promoted mineralization. The miR-17-5p expression was upregulated and ANKH was down-regulated in the aortic arteries with calcification.\u0000\u0000\u0000CONCLUSION\u0000Our data showed that miR-17-5p may promote vascular calcification by inhibiting ANKH expression.","PeriodicalId":10879,"journal":{"name":"Current neurovascular research","volume":" ","pages":""},"PeriodicalIF":2.1,"publicationDate":"2022-03-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41925408","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Background and objective: The potential impact of rebleeding and Delayed Cerebral Ischemia (DCI) on long-term survival in patients with aneurysmal subarachnoid hemorrhage (aSAH) remained unclear. This study aimed to investigate whether DCI and rebleeding increase the risk of long-term all-cause mortality in patients with aSAH who survived the follow-up period of one year.
Methods: We retrospectively collected data on patients with atraumatic aSAH who were still alive 12 months after aSAH occurrence between December 2013 and June 2019 from the electronic health system. Patients were then classified by the occurrence of rebleeding or DCI during hospitalization. Death records were obtained from an administrative database, the Chinese Household Registration Administration System, until April 20, 2021. Multivariable Cox proportional hazards models were used to compare overall survival in different groups. Sensitivity analysis was performed with propensity-score matching (PSM).
Results: A total of 2,607 patients were alive one year after aSAH. The crude annual death rate from any cause among patients who had rebleeding (7.2 per 100 person-years) and patients who had DCI (3.7 per 100 person-years) during hospitalization was higher than that of patients with neither event (2.1 per 100 person-years). Multivariate analysis showed that rebleeding is an independent risk factor for long-term mortality (adjusted hazard ratio (aHR), 2.37; 95% confidence interval (CI), 1.47- 3.81). DCI was an independent prognostic factor of poorer overall survival (aHR, 2.09; 95% CI, 1.54-2.84).
Conclusion: Amongst patients alive one year after aSAH, rebleeding and DCI during hospitalization were independently associated with higher rates of long-term mortality.
{"title":"Association of Rebleeding and Delayed Cerebral Ischemia with Long-term Mortality Among 1-year Survivors After Aneurysmal Subarachnoid Hemorrhage.","authors":"Xing Wang, Yu Zhang, Weelic Chong, Yang Hai, Peng Wang, Haidong Deng, Chao You, Fang Fang","doi":"10.2174/1567202619666220822105510","DOIUrl":"https://doi.org/10.2174/1567202619666220822105510","url":null,"abstract":"<p><strong>Background and objective: </strong>The potential impact of rebleeding and Delayed Cerebral Ischemia (DCI) on long-term survival in patients with aneurysmal subarachnoid hemorrhage (aSAH) remained unclear. This study aimed to investigate whether DCI and rebleeding increase the risk of long-term all-cause mortality in patients with aSAH who survived the follow-up period of one year.</p><p><strong>Methods: </strong>We retrospectively collected data on patients with atraumatic aSAH who were still alive 12 months after aSAH occurrence between December 2013 and June 2019 from the electronic health system. Patients were then classified by the occurrence of rebleeding or DCI during hospitalization. Death records were obtained from an administrative database, the Chinese Household Registration Administration System, until April 20, 2021. Multivariable Cox proportional hazards models were used to compare overall survival in different groups. Sensitivity analysis was performed with propensity-score matching (PSM).</p><p><strong>Results: </strong>A total of 2,607 patients were alive one year after aSAH. The crude annual death rate from any cause among patients who had rebleeding (7.2 per 100 person-years) and patients who had DCI (3.7 per 100 person-years) during hospitalization was higher than that of patients with neither event (2.1 per 100 person-years). Multivariate analysis showed that rebleeding is an independent risk factor for long-term mortality (adjusted hazard ratio (aHR), 2.37; 95% confidence interval (CI), 1.47- 3.81). DCI was an independent prognostic factor of poorer overall survival (aHR, 2.09; 95% CI, 1.54-2.84).</p><p><strong>Conclusion: </strong>Amongst patients alive one year after aSAH, rebleeding and DCI during hospitalization were independently associated with higher rates of long-term mortality.</p>","PeriodicalId":10879,"journal":{"name":"Current neurovascular research","volume":"19 3","pages":"282-292"},"PeriodicalIF":2.1,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9253498","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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