伺服工作台的修正输入法误差前馈补偿控制

针对特殊形面的高效加工制造，开发了精密快速伺服工作台。在对系统模型进行分析的基础上，对伺服装置进行了ＰＩＤ校正，并提出和实现了修正输入法误差前馈补偿控制，理论分析表明，该控制方法可明显提高系统的精度和动态性能。对批量生产零件具有输入再现性的系统，实施该控制方法无需解析系统的精确模型，也无需占用计算机的实时运算时间，只需通过一次预实验修改输入函数即可完成建模。应用于加工实验，最大加工误差由３６μｍ降低到７μｍ。实际应用表明，该控制方法具有较大的工程实用性和明显的技术效果。     

Alpha-CaMKII-dependent plasticity in the cortex is required for permanent memory

Cortical plasticity seems to be critical for the establishment of permanent memory traces. Little is known, however, about the molecular and cellular processes that support consolidation of memories in cortical networks. Here we show that mice heterozygous for a null mutation of alpha-calcium-calmodulin kinase II (alpha-CaMKII+/-) show normal learning and memory 1-3 days after training in two hippocampus-dependent tasks. However, their memory is severely impaired at longer retention delays (10-50 days). Consistent with this, we found that alpha-CaMKII+/- mice have impaired cortical, but not hippocampal, long-term potentiation. Our results represent a first step in unveiling the molecular and cellular mechanisms underlying the establishment of permanent memories, and they indicate that alpha-CaMKII may modulate the synaptic events required for the consolidation of memory traces in cortical networks.     

一种多层前馈网络计量经济建模方法

介绍了4种敏感性分析方法,给出了多层前馈网络计量经济模型正规化灵敏度的解析计算方法,进而利用灵敏度来进行多层前馈网络结构优化.结果表明了对多层前馈网络计量经济模型进行敏感性分析是一种有效识别敏感因素的方法.     

前馈网络的一种线性化快速学习算法

针对前馈神经网络的反向传播（ＢＰ）学习算法收敛速度慢的缺点,提出了一种新的学习算法即线性化快速学习算法。这种学习算法在神经网络学习的初期,采用标准ＢＰ学习算法。而当神经网络接近最优点时,由于此时其连接权重调节幅度很小,因此采用对各层神经元的非线性作用函数进行泰勒级数展开,并取其一阶展开式近似逼近原函数,从而使其非线性作用函数转化为线性作用函数,简化了网络学习过程的计算量,加速了网络的学习速度。文中最后给出了采用线性化算法与标准ＢＰ算法对正弦函数的学习过程。     

Platelet-derived growth factor-alpha receptor activation is required for human cytomegalovirus infection

Human cytomegalovirus (HCMV) is a ubiquitous human herpesvirus that can cause life-threatening disease in the fetus and the immunocompromised host. Upon attachment to the cell, the virus induces robust inflammatory, interferon- and growth-factor-like signalling. The mechanisms facilitating viral entry and gene expression are not clearly understood. Here we show that platelet-derived growth factor-alpha receptor (PDGFR-alpha) is specifically phosphorylated by both laboratory and clinical isolates of HCMV in various human cell types, resulting in activation of the phosphoinositide-3-kinase (PI(3)K) signalling pathway. Upon stimulation by HCMV, tyrosine-phosphorylated PDGFR-alpha associated with the p85 regulatory subunit of PI(3)K and induced protein kinase B (also known as Akt) phosphorylation, similar to the genuine ligand, PDGF-AA. Cells in which PDGFR-alpha was genetically deleted or functionally blocked were non-permissive to HCMV entry, viral gene expression or infectious virus production. Re-introducing human PDGFRA gene into knockout cells restored susceptibility to viral entry and essential viral gene expression. Blockade of receptor function with a humanized PDGFR-alpha blocking antibody (IMC-3G3) or targeted inhibition of its kinase activity with a small molecule (Gleevec) completely inhibited HCMV viral internalization and gene expression in human epithelial, endothelial and fibroblast cells. Viral entry in cells harbouring endogenous PDGFR-alpha was competitively inhibited by pretreatment with PDGF-AA. We further demonstrate that HCMV glycoprotein B directly interacts with PDGFR-alpha, resulting in receptor tyrosine phosphorylation, and that glycoprotein B neutralizing antibodies inhibit HCMV-induced PDGFR-alpha phosphorylation. Taken together, these data indicate that PDGFR-alpha is a critical receptor required for HCMV infection, and thus a target for novel anti-viral therapies.     

多层前馈神经网络的动态规划算法

利用动态规划来训练多层前馈网络，即逐层修改网络的权值。其算法采用有关文献提出的矩阵的广义逆的正交反向传播算法，经有限次迭代即可得到每一层的最优权值。     

前馈控制的帆船用H∞航向控制器

由于帆船具有非常严重的非线性和非最小相位特性,因而帆船用自动舵设计起来很困难.在处理这类问题上,H∞控制器是一个强有力的工具.但在这个方法中,由于指标的相互矛盾,选定灵敏度函数和补灵敏度函数是实际应用的难点,而前馈控制可以有效地解决这个问题.为此,在前馈控制设计中引人了镜像映射的方法来消除非最小相位的影响.     

两输入非线性前馈系统的镇定方法

为了便于构造两输入非线性前馈系统的镇定控制器,通过变换构造出与原系统等价的复数域低维单输入非线性前馈系统,再利用已有的单输入系统的控制方法对该等价系统设计一个复数域镇定控制器,采用逆变换得到原系统的两个镇定控制器,提出了将原系统转化为等价系统后再进行设计的镇定方法。用Lyapunov稳定性定理证明了闭环控制系统状态的渐进稳定性。结果表明:等价系统比原系统具有更少的输入和更低的维数,基于等价系统的设计方法降低了系统的分析难度,简化了控制器的设计步骤。     

Interleukin-2 signals during priming are required for secondary expansion of CD8+ memory T cells

Although interleukin-2 (IL-2) was initially characterized as the primary T-cell growth factor following in vitro activation, less is known about its role in shaping T-cell responses to acute infections in vivo. The use of IL-2- or IL-2-receptor-deficient mice is problematic owing to their early development of autoimmunity, attributable to the central role of IL-2 in the generation, maintenance and function of CD4+CD25+ regulatory T cells. To bypass these inherent difficulties, we have studied the effect of IL-2 on T-cell responses to acute infections by adopting a mixed chimaera strategy in which T cells lacking the high-affinity IL-2 receptor could be studied in an otherwise healthy mouse containing a full complement of regulatory T cells. Here we show that although IL-2 signalling to pathogen-specific CD8+ T cells affects the number of developing effector and memory cells very little, it is required for the generation of robust secondary responses. This is not due to an altered T-cell-receptor repertoire development or selection, and does not reflect an acute requirement for IL-2 during secondary activation and expansion. Rather, we demonstrate a previously unappreciated role for IL-2 during primary infection in programming the development of CD8+ memory T cells capable of full secondary expansion. These results have important implications for the development of vaccination or immunotherapeutic strategies aimed at boosting memory T-cell function.     

两输入非线性前馈系统的镇定方法

为了便于构造两输入非线性前馈系统的镇定控制器,通过变换构造出与原系统等价的复数域低维单输入非线性前馈系统,再利用已有的单输入系统的控制方法对该等价系统设计一个复数域镇定控制器,采用逆变换得到原系统的两个镇定控制器,提出了将原系统转化为等价系统后再进行设计的镇定方法。用Lyapunov稳定性定理证明了闭环控制系统状态的渐进稳定性。结果表明:等价系统比原系统具有更少的输入和更低的维数,基于等价系统的设计方法降低了系统的分析难度,简化了控制器的设计步骤。     

Local aggregation of hormone-receptor complexes is required for activation by epidermal growth factor.

An analogue of epidermal growth factor (EGF) which is virtually devoid of biological activity retains receptor binding activity but cannot form cell surface clusters or patches. Bivalent anti-EGF antibodies restore both bioactivity and patch formation. The sensitivity of fibroblasts to native EGF can also be enhanced greatly by these antibodies, especially in hormone-resistant cell lines.     

CD4+ T cells are required for secondary expansion and memory in CD8+ T lymphocytes

A long-standing paradox in cellular immunology concerns the conditional requirement for CD4+ T-helper (T(H)) cells in the priming of cytotoxic CD8+ T lymphocyte (CTL) responses in vivo. Whereas CTL responses against certain viruses can be primed in the absence of CD4+ T cells, others, such as those mediated through 'cross-priming' by host antigen-presenting cells, are dependent on T(H) cells. A clearer understanding of the contribution of T(H) cells to CTL development has been hampered by the fact that most T(H)-independent responses have been demonstrated ex vivo as primary cytotoxic effectors, whereas T(H)-dependent responses generally require secondary in vitro re-stimulation for their detection. Here, we have monitored the primary and secondary responses of T(H)-dependent and T(H)-independent CTLs and find in both cases that CD4+ T cells are dispensable for primary expansion of CD8+ T cells and their differentiation into cytotoxic effectors. However, secondary CTL expansion (that is, a secondary response upon re-encounter with antigen) is wholly dependent on the presence of T(H) cells during, but not after, priming. Our results demonstrate that T-cell help is 'programmed' into CD8+ T cells during priming, conferring on these cells a hallmark of immune response memory: the capacity for functional expansion on re-encounter with antigen.     

Neuronal growth inhibitory factor inhibits pheochromocytoma PC12 in vitro

Neuronal growth inhibitory factor (GIF), named Metallothioneins-Ⅲ (MT-Ⅲ), is the first protein validated to be capable of inhibiting the growth of neurons in nervous system. We have detected the effects of recombinant GIF on the growth of neuroblastoma SY5Y and pheochromocytoma PC12 by the MTT (Thiazolyl blue) reduction assay. Recombinant GIF inhibited PC12 in vitro; the inhibitory rate was about 25% when GIF was at 100 mg/L; and the inhibitory rate was about 50% when GIF was at 300 mg/L. It is shown that PC12 could serve as a proper model for detecting neuronal growth inhibitory activity of GIF. Recombinant GIF did not inhibit neuroblastoma SY5Y in vitro, a common model of neuroma; it is also shown that GIF could not inhibit neuromata extensively. The reason for GIF inhibiting PC12 may be that PC12 have some properties of cholinergic neuron. It must play an important role in discovering the mechanism of GIF’s neuronal growth inhibitory activity.     

Neuronal growth inhibitory factor inhibits pheochromo-cytoma PC12 in vitro

Neuronal growth inhibitory factor (GIF),named Metaliothioneins-Ⅲ (MT-Ⅲ), is the first protein validated to be capable of inhibiting the growth of neurons in nervous system. We have detected the effects of recombinant GIF on the growth of neuroblastoma SY5Y and pheochromocytoma PC12 by the MTT (Thiazolyl blue) reduction assay. Recombinant GIF inhibited PC12 in vitro; the inhibitory rate was about 25% when GIF was at 100 mg/L; and the inhibitory rate was about 50% when GIF was at 300 mg/L. It is shown that PC12 could serve as a proper model for detecting neuronal growth inhibitory activity of GIF. Recombinant GIF did not inhibit neuroblastoma SY5Y in vitro, a common model of neuroma; it is also shown that GIF could not inhibit neuromata extensively. The reason for GIF inhibiting PC12 may be that PC12 have some properties of cholinergic neuron. It must play an important role in discovering the mechanism of GIF's neuronal growth inhibitory activity.``     

Leukaemia inhibitory factor is identical to the myeloid growth factor human interleukin for DA cells

Leukaemia inhibitory factor (LIF) is a cytokine that induces macrophage differentiation of the murine M1 myeloid leukaemia cell line. We have isolated a cDNA clone encoding a novel human haemopoietic growth factor, human interleukin for DA cells (HILDA) that supports the proliferation of the murine interleukin-3-dependent leukaemic cell line, DA-la (refs 3-5). HILDA proved to be identical to LIF. The demonstration that the differentiation factor LIF will also serve as a growth factor for at least one myeloid leukaemic cell line provides further evidence that the distinction between growth-promoting and differentiation-inducing activities are largely determined by the target cell type.     

非线性复杂前馈系统的全局镇定控制

基于嵌套侵润函数构造了镇定器,并证明其整体收敛性,推广了该类前馈非线性系统控制器的应用范围.     

前馈神经网络盲信号分离的实验研究

介绍一个实现盲信号分离的前馈式神经网络的电路结构，并给出了电路在线性混合和动态混合情况下的测试结果。     

Raf-1 protein kinase is required for growth of induced NIH/3T3 cells

Many growth factors regulate the cytoplasmic Raf-1 protein kinase, consistent with its having a central role in transduction of growth signals. The kinase is ubiquitously expressed and can promote proliferation, presumably in a manner dependent on growth-factor receptors and membrane-associated oncogenes. We have now examined the dependence of serum- and TPA (12-O-tetradecanoylphorbol-13-acetate)-regulated NIH/3T3 cell growth on RAF-1 kinase to determine whether Raf-1 is essential for receptor signalling. We inhibited Raf-1 function by expressing c-raf-1 antisense RNA or kinase-defective c-raf-1 mutants. Antisense RNA for c-raf-1 interferes with proliferation of normal NIH/3T3 cells and reverts raf-transformed cells. In revertant cells, DNA replication induced by serum or TPA was eliminated or reduced proportionately to the reduction in Raf protein levels. Expression of a kinase-defective Raf-1 mutant (craf301) or a regulatory domain fragment (HCR) inhibited serum-induced NIH/3T3-cell proliferation and raf transformation even more efficiently. Inhibition by antisense RNA or craf301 blocked proliferation and transformation by Ki- and Ha-ras oncogenes. We conclude that raf functions as an essential signal transducer downstream of serum growth factor receptors, protein kinase C and ras.     

精准医疗中的柔性电子技术

 精准医疗是一种以个人健康大数据为诊疗依据的高度个性化的新型医疗模式,其依靠的数据主要包括基因型数据、表型数据和环境数据,其中表型数据和环境数据的获取需要借助具有动态数据采集能力的移动测量装置。本文简述了精准医疗的一般概念,提出柔性电子技术能够为动态医学监测提供有力的技术保障,并从材料体系、结构设计、集成方式和数据传递方式等方面概述了柔性电子技术,结合了目前柔性电子技术在医学监测领域的研究成果展示了其在精准医疗领域的巨大应用潜力。提出可以从提高系统的供电能力、提高系统的集成度与复杂度以及深入研究化学量检测等方面进一步提升柔性医学监测系统的性能,使其更好地服务于精准医疗模式。