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Small Interference RNA Targeting Connexin-43 Improves Motor Function and Limits Astrogliosis After Juvenile Traumatic Brain Injury.
ASN Neuro ( IF 3.9 ) Pub Date : 2019-06-13 , DOI: 10.1177/1759091419847090
Aleksandra Ichkova 1 , Andrew M Fukuda 2, 3, 4 , Nina Nishiyama 3 , Germaine Paris 3 , Andre Obenaus 3, 5, 6 , Jerome Badaut 1, 2, 3
Affiliation  

In the United States, the annual incidence of nonmilitary-related traumatic brain injury (TBI) is approximately 1.7 million, of which 327,000 are hospitalized and 52,000 die (Faul et al., 2010). Juvenile TBI (jTBI), which is the leading cause of death and disability in children and adolescents, is an important concern because the population group most affected (emergency department visit, hospitalization, and death) are those younger than 5 years, followed by teenagers aged 15 to 19 years old (Faul et al., 2010). The consequences of jTBI are divided into primary and secondary injuries. The initial primary injury results from the direct and immediate biomechanical disruption of the brain tissue. The secondary injuries are part of the development of pathophysiology with delayed molecular mechanisms occurring at sites directly surrounding the impacted site and expanding toward regions remote from the initial impact site (Pop and Badaut, 2011; Plesnila, 2016). The primary injury can only be lessened by taking preemptive cautions, such as wearing helmets, so the goal of potential therapeutics is to minimize the damage caused by the secondary injuries (Morales et al., 2005). The major landmarks of the secondary injury cascade are blood–brain barrier (BBB) disruption and edema with cellular swelling (Pop and Badaut, 2011; Fukuda et al., 2012, 2013). Notably, cerebral edema remains the most significant predictor of poor outcome after injury and accounts for half of the morbidity and mortality after jTBI (Donkin and Vink, 2010; Fukuda et al., 2012, 2013). However, the molecular and cellular mechanisms in edema spread are not yet well understood, and there are no pharmacological treatments available (Clement et al., 2018).

中文翻译:

靶向Connexin-43的小干扰RNA可改善运动功能并限制青少年脑外伤后的星形胶质化。

在美国,非军事性脑外伤(TBI)的年发病率约为170万,其中327,000住院,52,000死亡(Faul et al。,2010)。青少年TBI(jTBI)是儿童和青少年死亡和残疾的主要原因,它是一个重要的问题,因为受影响最大的人群(急诊,住院和死亡)是5岁以下的人群,其次是青少年15至19岁(Faul等,2010)。jTBI的后果分为原发性和继发性伤害。最初的主要伤害是由脑组织的直接和即时生物力学破坏引起的。继发性损伤是病理生理学发展的一部分,其分子机制延迟发生在受累部位的周围,并向远离初始受累部位的区域扩展(Pop和Badaut,2011; Plesnila,2016)。只有采取诸如戴头盔之类的事前注意措施,才能减轻原发性伤害,因此,潜在治疗方法的目标是最大程度地减少由继发性伤害引起的伤害(Morales等,2005)。继发性损伤级联的主要标志是血脑屏障(BBB)破坏和水肿伴细胞肿胀(Pop和Badaut,2011; Fukuda等,2012,2013)。值得注意的是,脑水肿仍然是损伤后不良预后的最重要预测指标,占jTBI术后发病率和死亡率的一半(Donkin和Vink,2010; Fukuda等,2012年,2013年)。然而,尚未充分了解水肿扩散的分子和细胞机制,并且没有可用的药理疗法(Clement等人,2018)。
更新日期:2020-04-20
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