Computational model

计算模型
  • 文章类型: Journal Article
    小脑广泛涉及在自适应运动控制中的重要作用。迄今为止,有关小脑运动控制的许多计算研究都集中在相关的体系结构和学习算法上,以进一步了解小脑功能。在本文中,我们将重点转向通过不同运动行为产生的驱动小脑适应的信号。要做到这一点,我们通过计算研究小脑对视动反射(OKR)的贡献,用于图像稳定的视觉反馈控制方案。我们开发了小脑响应对激发OKR的世界速度信号的适应性的计算模型(在头部固定的实验实验室条件下研究OKR时,世界速度信号用于模拟头部速度信号)。结果表明,小脑模型学习的滤波器高度依赖于有色噪声世界速度激励信号的功率谱。因此,这里的关键发现是小脑滤波器由OKR激励信号的统计量决定。
    The cerebellum is widely implicated in having an important role in adaptive motor control. Many of the computational studies on cerebellar motor control to date have focused on the associated architecture and learning algorithms in an effort to further understand cerebellar function. In this paper we switch focus to the signals driving cerebellar adaptation that arise through different motor behavior. To do this, we investigate computationally the contribution of the cerebellum to the optokinetic reflex (OKR), a visual feedback control scheme for image stabilization. We develop a computational model of the adaptation of the cerebellar response to the world velocity signals that excite the OKR (where world velocity signals are used to emulate head velocity signals when studying the OKR in head-fixed experimental laboratory conditions). The results show that the filter learnt by the cerebellar model is highly dependent on the power spectrum of the colored noise world velocity excitation signal. Thus, the key finding here is that the cerebellar filter is determined by the statistics of the OKR excitation signal.
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  • 文章类型: Review
    人体骨骼具有显著的再生能力。然而,5-10%的骨折未能愈合并发展为不愈合,这是一种具有挑战性的骨科并发症,需要复杂且昂贵的治疗。这篇综述论文将讨论四种不同的计算模型,每个捕获不愈合的特定临床病例:由骨髓管扩孔和骨膜剥离引起的不愈合,由于较大的碎片间隙而导致不愈合,由于遗传性疾病[即NF1相关的先天性胫骨假关节炎(CPT)]导致的不愈合和由于机械超负荷导致的不愈合。一起,这四种计算模型能够捕获各种骨折不愈合类型的病因,并设计其新颖的治疗策略。需要进一步的研究来证实动物和人类环境中的计算模型,并将它们从工作台转换到床边。
    The human skeleton has a remarkable regeneration capacity. Nevertheless, 5-10 % of the bone fractures fails to heal and develops into a non-union which is a challenging orthopedic complication requiring complex and expensive treatment. This review paper will discuss four different computational models, each capturing a particular clinical case of non-union: non-union induced by reaming of the marrow canal and periosteal stripping, non-union due to a large interfragmentary gap, non-union due to a genetic disorder [i.e. NF1 related congenital pseudoarthrosis of the tibia (CPT)] and non-union due to mechanical overload. Together, the four computational models are able to capture the etiology of a wide range of fracture non-union types and design novel treatment strategies thereof. Further research is required to corroborate the computational models in both animal and human settings and translate them from bench to bed side.
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