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国家自然科学基金(81370185)

作品数:12 被引量:40H指数:4
相关作者:刘辉国任洁袁晓王志华朱蝶更多>>
相关机构:华中科技大学华中科技大学同济医学院附属同济医院更多>>
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相关领域:医药卫生生物学机械工程更多>>

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降主动脉壁间血肿伴穿透性溃疡致咯血一例
2015年
患者男,66岁.因"间断咳嗽、咯血1个月余,再发1d"于2014年9月24日在武汉市同济医院就诊.患者2014年8月初因劳累后间断出现咳嗽、咳少量白色黏痰,痰中带血,至当地卫生院就诊,给予中药治疗(具体不详),症状改善不明显,仍有间断咯血.2014年8月22日患者咯血量明显增多,大口鲜红色血液,最多达100 ml/次,于当地医院就诊,给予抗感染(头孢替唑、左氧氟沙星)、止血(血凝酶、乙酰甘氨酸乙二胺、垂体后叶素)等治疗.
潘月影刘辉国
关键词:咯血量穿透性溃疡降主动脉间断咳嗽痰中带血
Altered Wnt Signaling Pathway in Cognitive Impairment Caused by Chronic Intermittent Hypoxia: Focus on Glycogen Synthase Kinase-3β and β-catenin被引量:14
2016年
Background: Cognitive impairment is a severe complication caused by obstructive sleep apnea (OSA). The mechanisms of causation are still unclear. The Wntβ-catenin signaling pathway is involved in cognition, and abnormalities in it are implicated in neurological disorders. Here, we explored the Wntβ-catenin signaling pathway abnormalities caused by chronic intermittent hypoxia (CIH), the most characteristic pathophysiological component of OSA. Methods: We divided 32 4-week-old male C57/BL mice into four groups of eight each: a CIH + normal saline (NS) group, CIH + LiCI group, sham CIH + NS group, and a sham CIH + LiCI group. The spatial learning performance of each group was assessed by using the Morris water maze (MWM). Protein expressions of glycogen synthase kinase-β (GSK-β) and β-catenin in the hippocampus were examined using the Western blotting test. EdU labeling and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling staining methods were used, respectively, to determine the proliferation and apoptosis of neurons in the hippocampal dentate gyrus region. Results: Mice exposed to CIH showed impaired spatial learning performance in the MWM, including increased mean escape latencies to reach the target platform, decreased mean times passing through the target platform and mean duration in the target quadrant. The GSK-313 activity increased, and expression of β-catenin decreased significantly in the hippocampus of the CIH-exposed mice. Besides, CIH significantly increased hippocampal neuronal apoptosis, with an elevated apoptosis index. Meanwhile, LiCI decreased the activity of GSK-β and increased the expression of β-catenin and partially reversed the spatial memory deficits in MWM and the apoptosis caused by CIH. Conclusions: Wntβ-catenin signaling pathway abnormalities possibly play an important role in the development of cognitive deficits among mice exposed to CIH and that LiCI might attenuate CIH-induced cognitive impairment via Wntβ-c
Yue-Ying PanYan DengSheng XieZhi-Hua WangYuWangJie RenHui-Guo Liu
关键词:Β-CATENIN
P2X7 Receptor Antagonism Attenuates the Intermittent Hypoxia-induced Spatial Deficits in a Murine Model of Sleep Apnea Via Inhibiting Neuroinflammation and Oxidative Stress被引量:7
2015年
Background:The mechanism of the neural injury caused by chronic intermittent hypoxia (CIH) that characterizes obstructive sleep apnea syndrome (OSAS) is not clearly known.The purpose of this study was to investigate whether P2X7 receptor (P2X7R) is responsible for the CIH-induced neural injury and the possible pathway it involves.Methods:Eight-week-old male C57BL/6 mice were used.For each exposure time point,eight mice divided in room air (RA) and IH group were assigned to the study of P2X7R expression.Whereas in the 21 days-Brilliant Blue G (BBG,a selective P2X7R antagonist) study,48 mice were randomly divided into CIH group,BBG-treated CIH group,RA group and BBG-treated RA group.The hippocampus P2X7R expression was determined by Western blotting and real-time polymerase chain reaction (PCR).The spatial learning was analyzed by Morris water maze.The nuclear factor kappa B (NFκB) and NADPH oxidase 2 (NOX2) expressions were analyzed by Westem blotting.The expressions of tumor necrosis factor α,interleukin 1 β (IL-β),IL-18,and IL-6 were measured by real-time PCR.The malondialdehyde and superoxide dismutase levels were detected by colorimetric method.Cell damage was evaluated by Hematoxylin and Eosin staining and Terminal Transferase dUTP Nick-end Labeling method.Results:The P2X7R mRNA was elevated and sustained after 3-day IH exposure and the P2X7R protein was elevated and sustained after 7-day IH exposure.In the BBG study,the CIH mice showed severer neuronal cell damage and poorer performance in the behavior test.The increased NFκB and NOX2 expressions along with the inflammation injury and oxidative stress were also observed in the CIH group.BBG alleviated CIH-induced neural injury and consequent functional deficits.Conclusions:The P2X7R antagonism attenuates the CIH-induced neuroinflammation,oxidative stress,and spatial deficits,demonstrating that the P2X7R is an important therapeutic target in the cognition deficits accompanied OSAS.
Yan Deng Xue-Ling Guo Xiao Yuan Jin Shang Die Zhu Hui-Guo Liu
关键词:INFLAMMATION
阻塞性睡眠呼吸暂停综合征患者认知功能障碍被引量:4
2015年
阻塞性睡眠呼吸暂停综合征(Obstructive Sleep Apnea Syndrome, OSAS)是当今社会常见的睡眠障碍相关呼吸系统疾病,国外报道 OSAS 的患病率为2%~4%,发病率随年龄的增长而增加[1]。因睡眠时反复发生的上呼吸道塌陷阻塞,导致慢性间歇缺氧和睡眠片段化,患者常表现为打鼾、自觉窒息而觉醒、白天睡眠增多、注意力难以集中等。目前越来越多的证据表明 OSAS 可引起患者不同程度的认知功能障碍,从而影响正常的生活和工作。本文就 OS-AS 引起认知功能障碍的研究进展进行综述。
潘月影刘辉国
关键词:阻塞性睡眠呼吸暂停综合征认知功能障碍呼吸系统疾病OSAS睡眠障碍
肥胖低通气综合征与阻塞性睡眠呼吸暂停低通气综合征的异与同被引量:6
2014年
肥胖是人类的痼疾,肥胖除本身给人体带来的种种不便之外,众多与肥胖密切相关的疾病也在严重危及着人类的健康。肥胖低通气综合征(obesityhypoventilationsyndrome,OHS)是一种与肥胖密切相关的呼吸障碍性疾病,因其独特的病理生理机制以及可能继发的心脑血管疾患而受到越来越多的重视。无独有偶,另外一种与肥胖密切关联的呼吸系统疾患,阻塞性睡眠呼吸暂停低通气综合征(obstructivesleepapneasyndrome,OSAS)与OHS之间也存在着千丝万缕的联系,两者在发病原因、病理生理学机制以及临床表现等方面,
刘辉国袁晓
关键词:阻塞性睡眠呼吸暂停低通气综合征肥胖低通气综合征病理生理学机制障碍性疾病心脑血管疾患呼吸系统疾患
阻塞性睡眠呼吸暂停与支气管哮喘的关系研究进展被引量:1
2016年
阻塞性睡眠呼吸暂停(obstructive sleep apnea,OSA)其特点是睡眠时反复上气道塌陷导致呼吸暂停和(或)低通气,引起间歇性低氧,表现为血氧饱和度下降和睡眠结构紊乱,从而产生相对睡眠剥夺和日间疲倦。
任洁刘辉国
关键词:阻塞性睡眠呼吸暂停支气管哮喘睡眠结构紊乱间歇性低氧低通气上气道
Regulatory Effects of AT1R-TRAF6-MAPKs Signaling on Proliferation of Intermittent Hypoxia-induced Human Umbilical Vein Endothelial Cells
2015年
Summary: Endothelial dysfunction induced by intermittent hypoxia (IH) participates in obstructive sleep apnea syndrome (OSAS)-associated cardiovascular disorders. Myeloid differentiation primary response 88 (MyD88) and tumor necrosis factor receptor-associated factor 6 (TRAF6) regulate nu- merous downstream adaptors like mitogen-activated protein kinases (MAPKs) and the subsequent oxidative stress and inflammatory responses. This study aimed to characterize the role of MyD88/TRAF6 in IH-treated cell function and its associated signaling. Human umbilical vein endo- thelial cells (HUVECs) were randomly exposed to IH or normoxia for 0, 2, 4 and 6 h. Western blot- ting was used to detect the expression pattern of target gene proteins [angiotensin 1 receptor (AT1R), p-ERK1/2, p-p38MAPK, MyD88 and TRAF6], and the relationships among these target genes down-regulated by the corresponding inhibitors were studied. Finally, the influence of these target genes on proliferation of HUVECs was also assessed by EdU analysis. Protein levels of AT1R, TRAF6 and p-ERK1/2 were increased after IH exposure, with a slight rise in MyD88 and a dynamic change in p-p38MAPK. The down-regulation of TRAF6 by siRNA reduced ERK1/2 phosphorylation during IH without any effects on ATIR. Blockade of AT1R with valsartan decreased TRAF6 and p-ERK1/2 protein expression after IH exposure. ERK1/2 inhibition with PD98059 suppressed only AT1R expression. IH promoted HUVECs proliferation, which was significantly suppressed by the in- hibition of TRAF6, AT1R and ERK1/2. The findings demonstrate that TRAF6 regulates the prolifera- tion of HUVECs exposed to short-term IH by modulating cell signaling involving ERK1/2 down- stream of AT1R. Targeting the AT1R-TRAF6-p-ERK1/2 signaling pathway might be helpful in re- storing endothelial function.
尚进郭雪玲邓燕袁晓刘辉国
Atorvastatin Attenuates Myocardial Hypertrophy Induced by Chronic Intermittent Hypoxia In Vitro Partly through miR-31/PKCε Pathway被引量:4
2018年
Atorvastatin is proven to ameliorate cardiac hypertrophy induced by chronic intermittent hypoxia (CIH). However, little is known about the mechanism by which atorvastatin modulates CIH-induced cardiac hypertrophy, and whether specific hypertrophyrelated microRNAs are involved in the modulation. MiR-31 plays key roles in the development of cardiac hypertrophy induced by ischemia/hypoxia. This study examined whether miR-31 was involved in the protective role of atorvastatin against CIH-induced myocardial hypertrophy. H9c2 cells were subjected to 8-h intermittent hypoxia per day in the presence or absence of atorvastatin for 5 days. The size of cardiomyocytes, and the expression of caspase 3 and miR-31 were determined by Western blotting and RT-PCR, respectively. MiR-31 mimic or Ro 31-8220, a specific inhibitor of protein kinase C epsilon (PKCε), was used to determine the role of miR-31 in the anti-hypertrophic effect of atorvastatin on cardiomyocytes. PKCε in the cardiomyocytes with miR-31 upregulation or downregulation was detected using RT-PCR and Western blotting. The results showed that CIH induced obvious enlargement of cardiomyocytes, which was paralleled with increased atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and slow/beta cardiac myosin heavy-chain (MYHT) mRNA levels. All these changes were reversed by the treatment with atorvastatin. Meanwhile, miR-31 was increased by CIH in vitro. Of note, the atorvastatin pretreatment significantly increased the mRNA and protein expression of PKCε and decreased that of miR-31. Moreover, overexpression of miR-31 abolished the anti-hypertrophic effect of atorvastatin on cardiomyocytes. Upregulation and downregulation of miR-31 respectively decreased and increased the mRNA and protein expression of PKCε. These results suggest that atorvastatin provides the cardioprotective effects against CIH probably via up-regulating PKCε and down-regulating miR-31.
Jie RENWei LIUGuang-cai LIMeng JINZhen-xi YOUHui-guo LIUYi HU
关键词:ATORVASTATIN
慢性间歇低氧患者勃起功能障碍与氧化应激的关系研究进展
2014年
阻塞性睡眠呼吸暂停综合征(obstructivesleepapneasyndrome,OSAS)是由多种原因引起的睡眠中上气道阻塞,以睡眠中反复发生的呼吸变浅或暂停及日间嗜睡、疲乏等为特征的常见综合征。OSAS患者由于反复发作的短暂阻塞性呼吸暂停、低通气、血氧饱和度下降、胸内压波动、睡眠结构紊乱、神经内分泌改变及微觉醒等,可导致全身各个系统的损伤,包括性功能障碍。
朱蝶刘辉国
关键词:OSAS患者阻塞性睡眠呼吸暂停综合征勃起功能障碍慢性间歇低氧氧化应激睡眠结构紊乱
阻塞性睡眠呼吸暂停综合征炎症反应基因的研究进展被引量:3
2016年
阻塞性睡眠呼吸暂停综合征(OSAS)是指睡眠时反复发生上呼吸道部分或完全性阻塞,导致气流中断(呼吸暂停)或减少(低通气),引起血氧饱和度下降和高碳酸血症,随后发生微觉醒的睡眠呼吸障碍性疾病.患者一般表现为疲劳和白天嗜睡,注意力或记忆力减退及睡眠打鼾史[1].呼吸暂停低通气指数(AHI)是目前国内外反映OSAS病情轻重的主要指标.根据AHI值可将OSAS分为轻度(5~15次/h)、中度(15 ~ 30次/h)和重度(≥30次/h),目前发现无论轻度OSAS患者有无表现出日间症状,均可能与心血管疾病发病率的显著增加相关2],而炎症反应在OSAS及其并发症发病机制中的作用越来越受到人们的重视.现对评估OSAS患者炎症反应的遗传学基础研究进展综述如下.
王志华刘辉国
关键词:阻塞性睡眠呼吸暂停综合征呼吸暂停低通气指数OSAS患者高碳酸血症血氧饱和度障碍性疾病
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