| 1 | Health Res Policy Syst 2010 -1 8: 28 |
|---|---|
| PMID | 20920289 |
| Title | Integrating clinicians, knowledge and data: expert-based cooperative analysis in healthcare decision support. |
| Abstract | Decision support in health systems is a highly difficult task, due to the inherent complexity of the process and structures involved. 本文介绍了一种新的基于专家合作分析（EBCA）的新型混合方法，该分析纳入了数据分析方法中的显式专家知识，并引起了隐式或TACIT专家知识（我知道) to improve decision support in healthcare systems. EbCA has been applied to two different case studies, showing its usability and versatility: 1) Bench-marking of small mental health areas based on technical efficiency estimated by EbCA-Data Envelopment Analysis (EbCA-DEA), and 2) Case-mix of精神分裂症基于基于规则（CLBR）聚类的功能依赖性。在这两种情况下，都使用定性明确的先验知识对经典程序进行比较。贝叶斯预测有效性度量用于与专家面板结果进行比较。在两种情况下，在“ 1”和kappa的情况下，通过类内相关系数测试了总体一致性。 EbCA is a new methodology composed by 6 steps:. 1) Data collection and data preparation; 2) acquisition of "Prior Expert Knowledge" (PEK) and design of the "Prior Knowledge Base" (PKB); 3) PKB-guided analysis; 4) support-interpretation tools to evaluate results and detect inconsistencies (here Implicit Knowledg -我知道- might be elicited); 5) incorporation of elicited我知道in PKB and repeat till a satisfactory solution; 6) post-processing results for decision support. EbCA has been useful for incorporating PEK in two different analysis methods (DEA and Clustering), applied respectively to assess technical efficiency of small mental health areas and for case-mix of精神分裂症基于功能依赖性。经典方法获得的结果差异主要与我知道which could be elicited by using EbCA and had major implications for the decision making in both cases. This paper presents EbCA and shows the convenience of completing classical data analysis with PEK as a mean to extract relevant knowledge in complex health domains. One of the major benefits of EbCA is iterative elicitation of我知道。。Both explicit and tacit or implicit expert knowledge are critical to guide the scientific analysis of very complex decisional problems as those found in health system research. |
| SCZ Keywords | 精神分裂症 |
| 2 | 神经毒理学2012年10月33日：1058-66 |
| PMID | 23227486 |
| Title | Effects of ketamine and its metabolites on ion currents in differentiated hippocampal H19-7 neuronal cells and in HEK293T cells transfected with ?-hslo subunit. |
| Abstract | 氯胺酮（KT）是一种解离性麻醉，已知会诱导精神分裂症-l我知道E精神病。尽管KT是一种受控药物，但KT滥用的百分比最近迅速增长。KT作用的机制与NMDA受体的抑制有关。KT是否对海马神经元中离子电流产生其他影响尚不清楚。在这项研究中，我们试图评估KT和其他相关化合物对海马神经元衍生的H19-7细胞中离子电流的可能影响。该药物对CA（2+）激活的K（+）电流产生了抑制作用（我知道（CA）在这些细胞中，IC（50）值为274？m。皮马酸（30？m）或Abietic Acid（30？m），已知会刺激大传导CA（2+）激活的K（+）通道，反转KT诱导的I（K）（K）（Ca）。在表达A-Humans低戳的HEK293T细胞中，KT诱导的I（K）（CA）的抑制仍然存在。脱氢甲苯丙胺（300？m）几乎没有影响我知道（CA）振幅，而甲苯丙胺（300？m）略有抑制。在内部？外构型中，kt应用于膜的细胞内面，并未改变大传导CA（2+） - 激活的K（+）（BKCA）通道的单个通道电导；但是，它确实显着降低了通道开口的可能性。KT的添加可有效降低电压门控Na（+）电流的峰值振幅。此外，发现KT的存在以增强分化H19-7细胞中膜电穿孔诱导的内向电流（IMEP）的幅度。通过进一步应用LACL（3）（100？m），而不是NMDA（30？m），可以反转KT刺激的IMEP。这种离子通道化合物的调节可能有助于基本机制，如果在体内发生类似的发现，则KT及其代谢产物会影响海马神经元的电行为。 |
| SCZ Keywords | 精神分裂症 |
| 3 | Front Pharmacol 2012 -1 3: 11 |
| PMID | 22347859 |
| Title | CYPPA是一种阳性SK3/SK2调节剂，可降低多巴胺能神经元的活性，抑制多巴胺释放，并抵消甲基化甲酯诱导的高多巴胺能行为。 |
| Abstract | 含有中脑神经元的多巴胺（DA）在几种精神病和神经系统疾病中起关键作用，包括精神分裂症以及注意力缺陷多动障碍，以及帕金森氏病选择性地退化的黑质nigra pars compacta神经元。DA受体和转运蛋白的药理调节是治疗与DA相关疾病的良好方法。通过影响这些自主射击神经元的放电模式来直接调节DA系统，尚未被用作潜在的治疗策略。小电导Ca（2+） - 激活的K（+）通道（SK通道），尤其是SK3亚型，在DA神经元的生理学中很重要，并且改变SK通道活性的药物可能会影响DA信号传导和与DA相关的行为。在这里，我们表明环己基 - [2-（3,5-二甲基 - 吡唑-1-基）-6-甲基 - 吡啶蛋白-4-基] - 胺（Cyppa），Sk3（SK3）的亚型选择性调节剂（SK3）？>？sk2？>？>？>？sk1，我知道），自发发射速率降低，增加了对阿瓜蛋白敏感后极光的持续时间，并引起了来自小鼠和大鼠中脑切片中DA神经元中电流诱发的作用电位的活性依赖性抑制。使用来自大鼠培养的DA神经元的免疫细胞化学和药理验证的DA释放测定，我们表明Cyppa以浓度依赖性方式抑制DA释放，其最大效应等于D2受体激动剂奎因螺旋体。体内研究表明，cyppa的全身给药减弱了甲化甲酯诱导的小鼠的多动症和刻板印象行为。综上所述，数据强调了SK3通道在DA神经元的生理学中所起的重要作用，并表明它们的CYPPA促进会深刻影响生理和药理诱导的高胺能行为。 |
| SCZ Keywords | 精神分裂症 |
| 4 | Am. J. Physiol., Cell Physiol. 2013 Jul 305: C197-206 |
| PMID | 23703525 |
| Title | neuregulin 1 / ErbB4信号调节Kv4.2-mediated transient outward K+ current through the Akt/mTOR pathway. |
| Abstract | Neuregulin-1 (NRG-1) is a member of a family of neurotrophic factors that is required for the differentiation, migration, and development of neurons. NRG-1 signaling is thought to contribute to both neuronal development and the neuropathology of精神分裂症, which is believed to be a neurodevelopmental disorder. However, few studies have investigated the role of NRG-1 on voltage-gated ion channels. In this study, we report that NRG-1 specifically increases the density of transient outward K(+) currents (IA) in rat cerebellar granule neurons (CGNs) in a time-dependent manner without modifying the activation or inactivation properties of IA channels. The increase in IA density is mediated by increased protein expression of Kv4.2, the main ?-subunit of the IA channel, most l我知道ely by upregulation of translation. The effect of NRG-1 on IA density and Kv4.2 expression was only significant in immature neurons. Mechanistically, both Akt and mammalian target of rapamycin (mTOR) signaling pathways are required for the increased NRG-1-induced IA density and expression of Kv4.2. Moreover, pharmacological blockade of the ErbB4 receptor reduced the effect of NRG-1 on IA density and Kv4.2 induction. Our data reveal, for the first time, that stimulation of ErbB4 signaling by NRG-1 upregulates the expression of K(+) channel proteins via activation of the Akt/mTOR signaling pathway and plays an important role in neuronal development and maturation. NRG1 does not acutely change IA and delayed-rectifier outward (我知道) of rat CGNs, suggesting that it may not alter excitability of immature neurons by altering potassium channel property. |
| SCZ Keywords | 精神分裂症 |