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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

Preterm neonatal brain injury: are human amnion epithelial stem cells a pan-treatment for neuroprotection and neurorepair?

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Neural Regeneration Research 2022年第6期17卷 1261-1262页

作者： Joanne O.Davidson Simerdeep K.Dhillon laura bennet Department of Physiology University of AucklandAucklandNew Zealand

Premature birth,defined as birth before 37 weeks completed gestation,represents 11.1%of all live births worldwide and the rate has increased in almost all countries over the past few decades(Dhillon et al.,2018).Although mortality after preterm birth has fallen steadily over time,preterm infants continue to have very high rates of neurodevelopmental disability,including severe motor disorders such as cerebral palsy(Dhillon et al.,2018;Yates et al.,2021).

关键词： birth repair steadily

Challenges in developing therapeutic strategies for mild neonatal encephalopathy

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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

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

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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

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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

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

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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

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)

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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

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

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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...