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本文引用的文献

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Three Reasons Not to Believe in an Autism Epidemic.不相信自闭症流行的三个理由。
Curr Dir Psychol Sci. 2005 Apr;14(2):55-58. doi: 10.1111/j.0963-7214.2005.00334.x.
2
Prevalence of autism spectrum disorders--Autism and Developmental Disabilities Monitoring Network, 14 sites, United States, 2008.自闭症谱系障碍的流行率——自闭症及发展障碍监测网络,美国 14 个监测点,2008 年。
MMWR Surveill Summ. 2012 Mar 30;61(3):1-19.
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Can pupil size and pupil responses during visual scanning contribute to the diagnosis of autism spectrum disorder in children?儿童视觉扫描过程中的瞳孔大小和瞳孔反应能否有助于自闭症谱系障碍的诊断?
J Psychiatr Res. 2011 Aug;45(8):1077-82. doi: 10.1016/j.jpsychires.2011.01.008. Epub 2011 Jun 15.
4
Enhanced cortisol response to stress in children in autism.自闭症儿童对应激的皮质醇反应增强。
J Autism Dev Disord. 2012 Jan;42(1):75-81. doi: 10.1007/s10803-011-1214-0.
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Theoretical aspects of autism: causes--a review.自闭症的理论方面:病因——综述。
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Altered ultrasonic vocalizations in a tuberous sclerosis mouse model of autism.自闭症结节性硬化症小鼠模型的超声发声异常。
Proc Natl Acad Sci U S A. 2010 Jun 15;107(24):11074-9. doi: 10.1073/pnas.1005620107. Epub 2010 Jun 1.
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Effect of propranolol on functional connectivity in autism spectrum disorder--a pilot study.普萘洛尔对自闭症谱系障碍功能连接的影响——一项初步研究。
Brain Imaging Behav. 2010 Jun;4(2):189-97. doi: 10.1007/s11682-010-9098-8.
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Recent advances in research on early detection, causes, biology, and treatment of autism spectrum disorders.自闭症谱系障碍早期检测、病因、生物学及治疗方面的最新研究进展。
Curr Opin Neurol. 2010 Apr;23(2):95-6. doi: 10.1097/WCO.0b013e3283377644.
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Advances in the early detection of autism.自闭症早期检测的进展。
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10
The prodrome of autism: early behavioral and biological signs, regression, peri- and post-natal development and genetics.自闭症的前驱期:早期行为和生物学特征、倒退、围产期和产后发育以及遗传学。
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自闭症谱系障碍患者瞳孔和唾液自主神经功能障碍的指标。

Pupil and salivary indicators of autonomic dysfunction in autism spectrum disorder.

机构信息

Life Span Institute, Neurocognitive Development of Autism Research Laboratory, The University of Kansas, 1000 Sunnyside Avenue, Room 1052, Lawrence, KS 66045, USA.

出版信息

Dev Psychobiol. 2013 Jul;55(5):465-82. doi: 10.1002/dev.21051. Epub 2012 May 29.

DOI:10.1002/dev.21051
PMID:22644965
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3832142/
Abstract

Dysregulated tonic pupil size has been reported in autism spectrum disorder (ASD). Among the possible sources of this dysregulation are disruptions in the feedback loop between norepinephrine (NE) and hypothalamic systems. In the current study, we examined afternoon levels of salivary alpha-amylase (sAA, a putative correlate of NE) and cortisol (used to assess stress-based responses) in two independent samples of children with ASD. We found a larger pupil size and lower sAA levels in ASD, compared to typical and clinical age-matched controls. This was substantiated at the individual level, as sAA levels were strongly correlated with tonic pupil size. Relatively little diurnal variation in sAA taken in the home environment in the ASD group was also observed, while typical controls showed a significant linear increase throughout the day. Results are discussed in terms of potential early biomarkers and the elucidation of underlying neural dysfunction in ASD.

摘要

在自闭症谱系障碍(ASD)中,已经报道了张力性瞳孔大小失调。这种失调的可能来源之一是去甲肾上腺素(NE)和下丘脑系统之间的反馈回路中断。在当前的研究中,我们检查了两个独立的 ASD 儿童样本中唾液淀粉酶(sAA,一种可能与 NE 相关的物质)和皮质醇(用于评估基于压力的反应)的下午水平。与典型和临床年龄匹配的对照组相比,我们发现 ASD 患者的瞳孔更大,sAA 水平更低。这在个体水平上得到了证实,因为 sAA 水平与张力性瞳孔大小呈强相关。在 ASD 组中,在家庭环境中采集的 sAA 昼夜变化相对较小,而典型对照组则在全天呈显著线性增加。结果从潜在的早期生物标志物和 ASD 中潜在的神经功能障碍的阐明方面进行了讨论。