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| 1 | Can we further optimize therapeutic hypothermia for hypoxic-ischemic encephalopathy?显示文摘Perinatal hypoxic-ischemic encephalopathy is a leading cause of neonatal death and disability.Therapeutic hypothermia significantly reduces death and major disability associated with hypoxic-ischemic encephalopathy;however,many infants still experience lifelong disabilities to movement,sensation and cognition.Clinical 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 encephalopathy.The clinical guidelines also recommend that infants be re warmed at a rate of 0.5℃ per hour,but this is not based on strong evidence.There are no randomized controlled trials investigating the optimal rate of rewarming after therapeutic hypothermia for infants with hypoxic-ischemic encephalopathy.Preclinical studies of rewarming are conflicting and results were confounded by treatment with sub-optimal durations of hypothermia.In 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. | Anthony Davies Guido Wassink Laura Bennet Alistair J.Gunn Joanne O.Davidson | 2019 | Neural Regeneration Research2019，14，10： | 20 |
| 2 | 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)显示文摘目的 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? | 曹云 Alistair Jan GUAN Laura BENNET David WU Sherly GEORGE Peter GLUCKMAN Jian GUAN 邵肖梅 | 2004 | 中国当代儿科杂志2004，6，6： | 1 |
| 3 | Glia and hemichannels: key mediators of perinatal encephalopathy显示文摘Perinatal encephalopathy remains a major cause of disability, such as cerebral palsy. Therapeutic hypothermia 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 mediated injury likely involve impaired intracellular 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. | Robert Galinsky Joanne O.Davidson Justin M.Dean Colin R.Green Laura Bennet Alistair J.Gunn | 2018 | Neural Regeneration Research2018，13，2： | 1 |
| 4 | Preterm neonatal brain injury: are human amnion epithelial stem cells a pan-treatment for neuroprotection and neurorepair?显示文摘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). | Joanne O.Davidson Simerdeep K.Dhillon Laura Bennet | 2022 | Neural Regeneration Research2022，17，6： | 1 |
| 5 | Challenges in developing therapeutic strategies for mild neonatal encephalopathy显示文摘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. | Alice McDouall Guido Wassink Laura Bennet Alistair J.Gunn Joanne O.Davidson | 2022 | Neural Regeneration Research2022，17，2： | 1 |
| 6 | Does MgSO_(4) protect the preterm brain?Dissecting its role in the pathophysiology of hypoxic ischemic encephalopathy显示文摘Mitigating preterm encephalopathy continues to be one of the greatest challenges in perinatal medicine.Preterm 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 lifetime.The cost of disability associated with preterm brain injury continues to rise.Prevention of this injury,and disability,would significantly reduce this socioeconomic burden. | Robert Galinsky Laura Bennet Alistair J.Gunn | 2024 | Neural Regeneration Research2024，19，9： | 0 |
| 7 | 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显示文摘目的 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。 | 骆菲 曹云 GUAN Jian GUNN Alistair Jan BENNET Laura GEORGE Sherly GLUCKMAN Peter 邵肖梅 陈莲 | 2007 | 中华围产医学杂志2007，10，5： | 0 |
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