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| 1 | A statistical explanation of MaxEnt for ecologists显示文摘 | JaneElith Steven J.Phillips TrevorHastie MiroslavDudík Yung EnChee Colin J.Yates | 2010 | Diversity and Distributions2010，，1： | 2 |
| 2 | A statistical explanation of MaxEnt for ecologists显示文摘 | JaneElith Steven J.Phillips TrevorHastie MiroslavDudík Yung EnChee Colin J.Yates | 2010 | Diversity and Distributions2010，，1： | 1 |
| 3 | Delayed treatment of secondary degeneration following acute optic nerve transection using a combination of ion channel inhibitors显示文摘Studies have shown that a combined application of several ion channel inhibitors immediately after central nervous system injury can inhibit secondary degeneration. However, for clinical use, it is necessary to determine how long after injury the combined treatment of several ion channel inhibitors can be delayed and efficacy maintained. In this study, we delivered Ca^(2+) entry-inhibiting P2X7 receptor antagonist oxidized-ATP and AMPA receptor antagonist YM872 to the optic nerve injury site via an iPRECIO~@ pump immediately, 6 hours, 24 hours and 7 days after partial optic nerve transection surgery. In addition, all of the ion channel inhibitor treated rats were administered with calcium channel antagonist lomerizine hydrochloride. It is important to note that as a result of implantation of the particular pumps required for programmable delivery of therapeutics directly to the injury site, seromas occurred in a significant proportion of animals, indicating infection around the pumps in these animals. Improvements in visual function were observed only when treatment was delayed by 6 hours; phosphorylated Tau was reduced when treatment was delayed by 24 hours or 7 days. Improvements in structure of node/paranode of Ranvier and reductions in oxidative stress indicators were also only observed when treatment was delayed for 6 hours, 24 hours, or 7 days. Benefits of ion channel inhibitors were only observed with time-delayed treatment, suggesting that delayed therapy of Ca^(2+) ion channel inhibitors produces better neuroprotective effects on secondary degeneration, at least in the presence of seromas. | Nathanael J.Yates Marcus K.Giacci Ryan L. O'Hare Doig Wissam Chiha Bethany E. Ashworth Jade Kenna Carole A. Bartlett Melinda Fitzgerald | 2017 | Neural Regeneration Research2017，12，2： | 0 |
| 4 | 运动不耐受诊断标准:Bárány协会分类委员会共识文件显示文摘我们提出了运动不耐受(motion sickness,MS),视觉诱发运动不耐受(visually induced motion sickness,VIMS),运动病(motion sickness disorder,MSD)和视觉诱发运动病(visually induced motion sickness disorder,VIMSD)的诊断标准,这些标准将被纳入国际前庭疾病分类。MS和VIMS是一种正常生理反应,几乎所有人都可能出现,但在某些情况下,个体对这种反应的易感性和严重性过高则被认为是一种疾病。本文提供了对由躯体运动或视觉运动引起的症状和体征的评价标准及个体反应严重程度是否可构成疾病诊断的指南。MS和VIMS的诊断标准包括由于暴露于躯体运动或视觉运动所引发的不良反应,通常导致在以下方面出现严重程度大于最低限度的症状或体征:恶心和/或胃肠道功能紊乱、体温调节功能紊乱、觉醒水平改变、头晕和/或眩晕、头痛和/或眼疲劳。这些症状/体征在暴露于运动状态时出现,随着暴露时间延长而加重,最终随运动结束而消失。当相同或相似的刺激反复诱发MS或VIMS发作,其严重程度在反复暴露后没有明显减轻,且因症状/体征而调整活动状态、避免参与诱发不耐受的运动刺激或负性情绪反应时,即可诊断为MSD和VIMSD。MS/MSD和VIMS/VIMSD可以单独出现,也可同时出现。由躯体运动或视觉运动刺激诱发的症状严重程度个体差异较大,并且同一个体也会因年龄、适应能力及合并疾病的变化而发生改变。本文探讨了评估MS症状的主要方法,易出现MS和VIMS相关情境以及导致易感性增加相关的个体特征。对上述环境和个人因素特征的准确评估及理解,将有助于MSD和VIMSD的诊断优化。 | 宋宁(译) 邢玥(译) 李康之(译) 金占国(审校) 杨旭(审校) Yoon-Hee Cha John F.Golding Behrang Keshavarz Joseph Furman Ji-Soo Kim Jose A.Lopez-Escamez Måns Magnusson Bill J.Yates Ben D.Lawson Jeffrey P.Staab(顾问) Alexandre Bisdorff(顾问) | 2022 | 神经损伤与功能重建2022，17，12： | 0 |
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