非局部条件积分方程在Banach空间中的可控性

利用Schauder不动点定理, 研究Banach空间中一类积分型微分方程的可控性. 针对Banach空间中带有非局部初值条件的积分系统, 建立了系统可控的充分条件, 并以一个具体的偏微分方程作为例子讨论了其可控性.     

广义次正定矩阵上的Oppenheim不等式

用矩阵分析的方法, 通过对广义次正定矩阵性质的进一步研究, 得到了更一般条件下的两个广义次正定矩阵的Hadamard乘积的行列式下界估计的Oppenheim不等式, 在适用范围和估计精度上都改进了已有的相应结果.     

基于两级神经网络的发酵过程多变量前馈解耦控制

针对具有时变、非线性、不确定性的多变量耦合生物发酵过程,提出了一种基于两级神经网络的多变量前馈解耦方法.一级神经网络利用可获得的过程信息拟和耦合通道的过程特性,实现耦合作用对被控量影响的估计;二级神经网络用来拟和控制通道的逆特性.通过两级网络的串联,消除系统间的耦合.实验结果表明,提出的解耦控制方法能适应生物发酵过程模型的不确定性和参数时变性,克服了前馈解耦方法依赖于过程模型和对模型参数的变化表现敏感的缺点.     

Prion protein cleavage fragments regulate adult neural stem cell quiescence through redox modulation of mitochondrial fission and SOD2 expression

Neurogenesis continues in the post-developmental brain throughout life. The ability to stimulate the production of new neurones requires both quiescent and actively proliferating pools of neural stem cells (NSCs). Actively proliferating NSCs ensure that neurogenic demand can be met, whilst the quiescent pool makes certain NSC reserves do not become depleted. The processes preserving the NSC quiescent pool are only just beginning to be defined. Herein, we identify a switch between NSC proliferation and quiescence through changing intracellular redox signalling. We show that N-terminal post-translational cleavage products of the prion protein (PrP) induce a quiescent state, halting NSC cellular growth, migration, and neurite outgrowth. Quiescence is initiated by the PrP cleavage products through reducing intracellular levels of reactive oxygen species. First, inhibition of redox signalling results in increased mitochondrial fission, which rapidly signals quiescence. Thereafter, quiescence is maintained through downstream increases in the expression and activity of superoxide dismutase-2 that reduces mitochondrial superoxide. We further observe that PrP is predominantly cleaved in quiescent NSCs indicating a homeostatic role for this cascade. Our findings provide new insight into the regulation of NSC quiescence, which potentially could influence brain health throughout adult life.     

Evidence of G-protein-coupled receptor and substrate transporter heteromerization at a single molecule level

G-protein-coupled receptors (GPCRs) can constitute complexes with non-GPCR integral membrane proteins, while such interaction has not been demonstrated at a single molecule level so far. We here investigated the potential interaction between the thyrotropin receptor (TSHR) and the monocarboxylate transporter 8 (MCT8), a member of the major facilitator superfamily (MFS), using fluorescence cross-correlation spectroscopy (FCCS). Both the proteins are expressed endogenously on the basolateral plasma membrane of the thyrocytes and are involved in stimulation of thyroid hormone production and release. Indeed, we demonstrate strong interaction between both the proteins which causes a suppressed activation of G_q/11 by TSH-stimulated TSHR. Thus, we provide not only evidence for a novel interaction between the TSHR and MCT8, but could also prove this interaction on a single molecule level. Moreover, this interaction forces biased signaling at the TSHR. These results are of general interest for both the GPCR and the MFS research fields.