检索结果-南通市图书馆

Neural Regeneration Research 2024年第9期19卷 1861-1862页

作者： Robert Galinsky Laura Bennet alistair J.gunn The Ritchie Centre Hudson Institute of Medical ResearchMelbourneVICAustralia Department of Obstetrics and Gynaecology Monash UniversityMelbourneVICAustralia Department of Physiology The University of AucklandAucklandNew Zealand

Mitigating preterm encephalopathy continues to be one of the greatest challenges in perinatal *** encephalopathy is associated with high mortality,serious morbidity,and significant socio-economic impacts on the individuals,their families,and public health sectors and welfare systems that last a *** cost of disability associated with preterm brain injury continues to *** of this injury,and disability,would significantly reduce this socioeconomic burden.

关键词： encephalopathy mortality hypoxic

选择性头部降温对胎羊缺血性脑损伤纹状体神经元凋亡和星形胶质细胞增殖的影响

在线全文

学校读者我要写书评

暂无评论

选择性头部降温对胎羊缺血性脑损伤纹状体神经元凋亡和星形胶质细...

选择性头部亚低温治疗对胎羊缺血性脑损伤纹状体神经元的保护作用

全国围产医学专题学术研讨会

作者：曹云骆菲 Guan Jian gunn alistair jan Bennet Laura George Sherly Gluckmap Peter 邵肖梅杨毅陈莲复旦大学儿科医院复旦大学妇产科医院新西兰奥克兰大学Liggins 研究所

围产期缺氧缺血性脑病(Hypoxia-Ischemia Encephalopathy,HIE)是引起神经系统后遗症的主要疾病, 它可引起纹状体多种表型的选择性神经元死亡,并改变神经递质的活性,从而引起神经系统后遗症。纹状体是锥体外系的主要部分和重要的运动整...

围产期缺氧缺血性脑病(Hypoxia-Ischemia Encephalopathy,HIE)是引起神经系统后遗症的主要疾病, 它可引起纹状体多种表型的选择性神经元死亡,并改变神经递质的活性,从而引起神经系统后遗症。纹状体是锥体外系的主要部分和重要的运动整合中枢,它调节肌张力、使运动协调,此部位又是缺氧敏感区,其损伤后遗症主要表现为锥体外系运动障碍,是 HIE 患儿运动功能障碍的主要原因。

关键词：

来源： cnki会议评论

在线全文

cnki会议

学校读者我要写书评

暂无评论

中华围产医学杂志 2007年第5期10卷 327-330,I0002-I0003页

作者：骆菲曹云 GUAN Jian gunn alistair jan BENNET Laura GEORGE Sherly GLUCKMAN Peter 邵肖梅陈莲复旦大学儿科医院新生儿科上海200032 新西兰奥克兰大学医学院Liggins研究所

目的研究选择性头部亚低温治疗对缺血性脑损伤胎羊纹状体不同表型神经元的保护作用。方法胎羊于妊娠117～124d（足月为147d）时通过双侧颈动脉阻塞30min造成双侧脑缺血损伤，通过冷循环水进行选择性头部亚低温治疗。将胎羊随机分为：... 详细信息

目的研究选择性头部亚低温治疗对缺血性脑损伤胎羊纹状体不同表型神经元的保护作用。方法胎羊于妊娠117～124d（足月为147d）时通过双侧颈动脉阻塞30min造成双侧脑缺血损伤，通过冷循环水进行选择性头部亚低温治疗。将胎羊随机分为：损伤组（n=10）、2h低温组（损伤后2h开始亚低温治疗，n=7）和6h低温组（损伤后6h开始亚低温治疗，n=8），另设假手术组（n=5）。用免疫组化法检测胎羊纹状体胆碱乙酰化酶（choline acetyltransferase，ChAT）标记的胆碱能神经元，谷氨酸脱羧酶（glutamate acid decarboxylase，GAD）、钙结合蛋白（calbindin-28kd）、神经肽Y（neuropeptide Y，NPY）标记的7氨基丁酸（gamma-aminobutyric acid，GABA）能神经元和神经型一氧化氮合酶（neuronal nitric oxide synthase，nNOS）标记的一氧化氮神经元的变化。结果假手术组ChAT、GAD、NPY和nNOS阳性神经元多，阳性染色主要位于胞质和树突内。损伤组纹状体ChAT阳性神经元为（118．10±74．33）个、GAD阳性神经元为（41．80±26．94）个、calbindin-28kd阳性神经元为（48．79±26．20）个／mm^2、NPY阳性神经元为（94．00±55．29）个、nNOS阳性神经元为（76．60±33．11）个，明显少于假手术组（P〈0．01）；在2h低温组明显多于损伤组（P〈0．05）；但6h低温组与损伤组差异无统计学意义。nNOS阳性神经元在2h低温组为（133．00±38．74）个，6h低温组为（127．38±68．18）个，明显多于损伤组（P〈0．05）。结论亚低温对胎羊缺血性脑损伤纹状体不同表型的神经元具有保护作用，这一作用与低温治疗开始的时间有关。亚低温治疗可能有助于改善围产期缺血性脑损伤引起的运动和认知功能障碍。

关键词：缺氧缺血,脑低温,人工纹状体神经元

Challenges in developing therapeutic strategies for mild neonatal encephalopathy

在线全文

学校读者我要写书评

暂无评论

Neural Regeneration Research 2022年第2期17卷 277-282页

作者： Alice McDouall Guido Wassink Laura Bennet alistair J.gunn Joanne O.Davidson Department of Physiology The University of AucklandAucklandNew Zealand

There is increasing evidence that infants with mild neonatal encephalopathy(NE) have significant risks of mortality, brain injury and adverse neurodevelopmental outcomes. In the era of therapeutic hypothermia, infants need to be diagnosed within 6 hours of birth, corresponding with the window of opportunity for treatment of moderate to severe NE, compared to the retrospective grading over 2 to 3 days, typically with imaging and formal electroencephalographic assessment in the pre-hypothermia era. This shift in diagnosis may have increased the apparent prevalence of brain damage and poor neurological outcomes seen in infants with mild NE in the era of hypothermia. Abnormal short term outcomes observed in infants with mild NE include seizures, abnormal neurologic examination at discharge, abnormal brain magnetic resonance imaging and difficulty feeding. At 2 to 3 years of age, mild NE has been associated with an increased risk of autism, language and cognitive deficits. There are no approved treatment strategies for these infants as they were not included in the initial randomized controlled trials for therapeutic hypothermia. However, there is already therapeutic creep, with many centers treating infants with mild NE despite the limited evidence for its safety and efficacy. The optimal duration of treatment and therapeutic window of opportunity for effective treatment need to be specifically established for mild NE as the evolution of injury is likely to be slower, based on preclinical data. Randomized controlled trials of therapeutic hypothermia for infants with mild NE are urgently required to establish the safety and efficacy of treatment. This review will examine the evidence for adverse outcomes after mild NE and dissect some of the challenges in developing therapeutic strategies for mild NE, before analyzing the evidence for therapeutic hypothermia and other strategies for treatment of these infants.

关键词： asphyxia electroencephalogram erythropoietin mild hypoxic ischemic encephalopathy neonatal encephalopathy neurological examination neuroprotection Sarnat score therapeutic hypothermia

Interleukin-1:an important target for perinatal neuroprotection?

在线全文

学校读者我要写书评

暂无评论

中国神经再生研究：英文版 2023年第1期18卷 47-50页

作者： Sharmony B.Kelly Elys Green Rod W.Hunt Claudia A.Nold-Petry alistair J.gunn Marcel F.Nold Robert Galinsky The Ritchie Centre Hudson Institute of Medical ResearchMelbourneVictoriaAustralia Department of Obstetrics and Gynaecology Monash UniversityVictoriaAustralia Department of Pediatrics Monash UniversityVictoriaAustralia Monash Newborn Monash Children’s HospitalMelbourneAustralia Department of Physiology The University of AucklandAucklandNew Zealand

Perinatal inflammation is a significant risk factor for lifelong neurodevelopmental impairments such as cerebral *** clinical and preclinical evidence links the severity and pattern of perinatal inflammation to impaired maturation of white and grey matters and reduced brain *** pathways are involved in the pathogenesis of perinatal ***,studies of human and experimental perinatal encephalopathy have demonstrated a strong causative link between perinatal encephalopathy and excessive production of the pro-inflammatory effector cytokine *** this review,we summarize clinical and preclinical evidence that underpins interleukin-1 as a critical factor in initiating and perpatuating systemic and central nervous system inflammation and subsequent perinatal brain *** also highlight the important role of endogenous interleukin-1 receptor antagonist in mitigating interleukin-1-driven neuroinflammation and tissue damage,and summarize outcomes from clinical and mechanistic animal studies that establish the commercially available interleukin-1 receptor antagonist,anakinra,as a safe and effective therapeutic *** reflect on the evidence supporting clinical translation of interleukin-1 receptor antagonist for infants at the greatest risk of perinatal inflammation and impaired neurodevelopment,and suggest a path to advance interleukin-1 receptor antagonist along the translational path for perinatal neuroprotection.

关键词： brain inflammation interleukin-1 receptor antagonist interleukin-1 interleukin-1β neonatal encephalopathy neuroprotection preterm brain injury

Can we further optimize therapeutic hypothermia for hypoxic-ischemic encephalopathy?

在线全文

学校读者我要写书评

暂无评论

Neural Regeneration Research 2019年第10期14卷 1678-1683页

作者： Anthony Davies Guido Wassink Laura Bennet alistair J.gunn Joanne O.Davidson Department of Physiology The University of Auckland

Perinatal hypoxic-ischemic encephalopathy is a leading cause of neonatal death and *** hypothermia significantly reduces death and major disability associated with hypoxic-ischemic encephalopathy;however,many infants still experience lifelong disabilities to movement,sensation and *** guidelines,based on strong clinical and preclinical evidence,recommend therapeutic hypothermia should be started within 6 hours of birth and continued for a period of 72 hours,with a target brain temperature of 33.5 ±0.5℃ for infants with moderate to severe hypoxic-ischemic *** clinical guidelines also recommend that infants be re warmed at a rate of 0.5℃ per hour,but this is not based on strong *** are no randomized controlled trials investigating the optimal rate of rewarming after therapeutic hypothermia for infants with hypoxic-ischemic *** studies of rewarming are conflicting and results were confounded by treatment with sub-optimal durations of *** this review,we evaluate the evidence for the optimal start time,duration and depth of hypothermia,and whether the rate of rewarming after treatment affects brain injury and neurological outcomes.

关键词： hypoxia-ischemia hypoxic-ischemic encephalopathy therapeutic hypothermia neuroprotection therapeutic strategies randomized controlled trials animal models fetal sheep piglets

Glia and hemichannels: key mediators of perinatal encephalopathy

在线全文

学校读者我要写书评

暂无评论

Neural Regeneration Research 2018年第2期13卷 181-189页

作者： Robert Galinsky Joanne O.Davidson Justin M.Dean Colin R.Green Laura Bennet alistair J.gunn Department of Physiology University of Auckland The Ritchie Centre Hudson Institute of Medical Research Department of Ophthalmology University of Auckland

Perinatal encephalopathy remains a major cause of disability, such as cerebral palsy. Therapeutic hypo- thermia is now well established to partially reduce risk of disability in late preterm/term infants. However, new and complementary therapeutic targets are needed to further improve outcomes. There is increasing evidence that glia play a key role in neural damage after hypoxia-ischemia and infection/inflammation. In this review, we discuss the role of astrocytic gap junction （connexin） hemichannels in the spread of neural injury after hypoxia-ischemia and/or infection/inflammation. Potential mechanisms of hemichannel medi- ated injury likely involve impaired intraceUular calcium handling, loss of blood-brain barrier integrity and release of adenosine triphosphate （ATP） resulting in over-activation of purinergic receptors. We propose the hypothesis that inflammation-induced opening of connexin hemichannels is a key regulating event that initiates a vicious cycle of excessive ATP release, which in turn propagates activation of purinergic receptors on microglia and astrocytes. This suggests that developing new neuroprotective strategies for preterm infants will benefit from a detailed understanding of glial and connexin hemichannel responses.

关键词： hypoxia-ischemia connexin hemichannels spreading injury connexin 43 astrocytes hypoxicischemic encephalopathy

胰岛素样生长因子-1减少胎羊缺血性脑白质损伤后淀粉样前体蛋白表达(英文)

在线全文

学校读者我要写书评

暂无评论

中国当代儿科杂志 2004年第6期6卷 449-452,F002页

作者：曹云 alistair jan GUAN Laura BENNET David WU Sherly GEORGE Peter GLUCKMAN Jian GUAN 邵肖梅复旦大学儿科医院新生儿科上海200032 The Liggin's Institute Faculty of Medicine and Health Science University of Auckland Auckland 92019 New Zealand

目的　淀粉样前体蛋白 (β APP)是脑白质损伤早期敏感的指标 ,并参与缺氧缺血性脑损伤机制。本研究观察胎羊缺血性脑白质损伤及胰岛素样生长因子 1(IGF 1)治疗对淀粉样前体蛋白 (β APP)表达的影响。方法　胎羊于胎龄 117 12 4天 (足月... 详细信息

目的　淀粉样前体蛋白 (β APP)是脑白质损伤早期敏感的指标 ,并参与缺氧缺血性脑损伤机制。本研究观察胎羊缺血性脑白质损伤及胰岛素样生长因子 1(IGF 1)治疗对淀粉样前体蛋白 (β APP)表达的影响。方法　胎羊于胎龄 117 12 4天 (足月为 14 7天 )时通过双侧颈动脉阻塞 30min造成双侧脑缺血损伤 ,损伤后胎羊随机分为损伤组 (n =8)和重组人IGF 1(rhIGF 1)治疗组 (n =9) ;另设正常对照组 (n =5 ) ,为假手术动物。治疗组缺血后 90min经侧脑室注射 3μgrhIGF 1;损伤组经侧脑室注射等量人工脑脊液。缺血损伤后 96h结束实验 ,处死动物 ,取出胎羊 ,固定脑组织。免疫组化法检测脑白质胶质原纤维酸性蛋白 (GFAP)、β APP阳性细胞及白质内髓鞘碱性蛋白 (MBP)密度。应用免疫荧光双标记观察APP表达阳性细胞。结果　与正常对照组 (2 7.8± 4 .8)比较 ,缺血损伤组MBP密度 (4.7± 7.1,P <0 .0 0 1)明显减少。正常对照组未见 β APP阳性细胞 ,损伤后阳性细胞数明显增加 (49.6± 2 3.7,P <0 .0 0 1) ,rhIGF 1治疗可减少 β APP阳性细胞数 (17.9± 16 .5 ,P <0 .0 1)。免疫荧光双标记显示部分细胞为 β APP GFAP双标阳性细胞。结论　胎羊缺血性脑白质损伤可导致星形胶质细胞表达β APP ,β APP表达增加可能与脑损伤有关?

关键词：胰岛素样生长因子-1 白质损伤 β-淀粉样前体蛋白胎羊

诊断性试验和策略的证据质量和推荐强度的分级

在线全文

学校读者我要写书评

暂无评论

中国循证医学杂志 2009年第5期9卷 503-508页

作者： Holger J Schünemann Andrew D Oxman jan Brozek Paul Glasziou Roman Jaeschke gunn E Vist John W Williams Jr Regina Kunz Jonathan Craig Victor M Montori Patrick Bossuyt Gordon H Guyatt 李晓黄程陈耀龙李幼平代表GRADE工作组

GRADE系统能对诊断性试验或策略的证据质量和推荐强度进行分级。本文旨在阐释在此过程中如何考虑患者的重要结局，

关键词：诊断性试验证据质量强度 E系统

GRADE指南：Ⅷ.证据质量评价--间接性

在线全文

学校读者我要写书评

暂无评论

中国循证医学杂志 2011年第12期11卷 1452-1458页

作者： Gordon Guyatt Andrew D.Oxman Regina Kunz James Woodcock jan Brozek Mark Helfand Pablo Alonso-Coello Yngve Falck-Ytter Roman Jaeschke gunn Vist Elie A.Akl Piet N Post Susan Norris Joerg Meerpohl Mona Nasser 代表GRADE工作组李幼平杨晓妍李鸿浩机构不详

直接证据来自直接比较我们关注的干预措施用于我们关注的患者人群,并测量患者重要结局的研究。间接证据可由以下4种方式之一产生。第一,患者可能与我们关注的患者不同(适用性一词常用于这类间接性)。第二,所检验的干预措施可能与我们关... 详细信息

直接证据来自直接比较我们关注的干预措施用于我们关注的患者人群,并测量患者重要结局的研究。间接证据可由以下4种方式之一产生。第一,患者可能与我们关注的患者不同(适用性一词常用于这类间接性)。第二,所检验的干预措施可能与我们关注的干预措施不同。有关患者和干预措施间接性的决策取决于对生物或社会因素差异是否大到可能使效应尺度出现预期的较大差异的考虑。第三,结果可能有别于最初设定的结局指标——如替代结果本身不重要,但测量之是基于替代结果的变化反映患者重要结局变化这一假设。第四类间接性在概念上与前三类不同,发生于临床医生必须在未经直接比较的两种干预措施间做出选择时。这种情况下比较治疗方案需要特定的统计方法,并根据患者人群、联合干预措施、结局测量指标及备选干预措施试验方法的差异程度,将证据级别降低1或2级。

关键词： GRADE 证据质量间接性间接比较适用性外部有效性