WWP2 promotes degradation of transcription factor OCT4 in human embryonic stem cells

POU 抄写因素 OCT4 不仅在维持 pluripotent 和房间而且幕作为通过基因剂量的一个房间命运决定因素完成的胚胎的茎(ES ) 的自我更新的状态起一个必要作用。然而，控制细胞内部的 OCT4 蛋白质水平的分子的机制留下逃犯。这里，我们报导那人的 WWP2， E3 ubiquitin (Ub ) 蛋白质 ligase，通过它的 WW 领域明确地与 OCT4 交往并且在 vitro 并且在 vivo 提高 OCT4 的 Ub 修正。我们首先证明在人的 ES 房间的内长的 OCT4 能被 Ub post-translationally 修改。而且，我们发现 WWP2 以一种剂量依赖者方式，和 WWP2 的活跃地点半胱氨酸残余通过 26S proteasome 支持了 OCT4 的降级在 OCT4 上为它的酶的活动和解朊的效果被要求。显著地，我们当 WWP2 表示是由特定的 RNA 干扰(RNAi ) 的 downregulated 时，内长的 OCT4 蛋白质水平显著地被提高的数据表演，建议那 WWP2 是为在人的 ES 房间维持合适的 OCT4 蛋白质水平的一个重要管理者。而且，北污点分析证明 WWP2 抄本在多样的人的织物 / 器官是广泛地在场的并且高度在无差别的人的 ES 房间表示了。然而，它的表示水平快速在区分的人的 ES 房间以后被减少，显示 WWP2 表示力量发展地被调整。我们的调查结果证明 WWP2 是在人的 ES 房间的 OCT4 蛋白质水平的一个重要管理者。

CONVEX MAPPINGS ASSOCIATED WITH THE ROPER-SUFFRIDGE EXTENSION OPERATOR

LetλG(z)|dz|be the hyperbolic metric on a simply connected proper domain G■C containing the origin,and let‖·‖j be the Banach norms of C^nj for j=1,2,…,k.This note is to prove that if f is a normalized biholomorphic convex function on G,thenΦN,1/p1,…,1/pk(f)(z)=F1/p1,…,1/pk(z)=f(z1),(f'(z1))^1/p1z,…,(f'(z1))^1/pkw)is a normalized biholomorphic convex mapping on ?N={(z1,z,…,w)∈C×C^n1×…×C^nk:‖z‖^p11+…+‖w‖^pkk<1/λG(z1)},where N=1+n1+…+nk and the branch is chosen such that (f'(z1))^1/pj|z1=0=1, j=1, …, k.Applying to the Roper-Suffridge extension operator,we obtain a new convex mappings construction of an unbounded domain and a refinement of convex mappings construction on a Reinhardt domain,respectively.

FreeformNet:fast and automatic generation of multiple-solution freeform imaging systems enabled by deep learning

Using freeform optical surfaces in lens design can lead to much higher system specifications and performance while significantly reducing volume and weight.However,because of the complexity of freeform surfaces,freeform optical design using traditional methods requires extensive human effort and sufficient design experience,while other design methods have limitations in design efficiency,simplicity,and versatility.Deep learning can solve these issues by summarizing design knowledge and applying it to design tasks with different system and structure parameters.We propose a deep-learning framework for designing freeform imaging systems.We generate the data set automatically using a combined sequential and random system evolution method.We combine supervised learning and unsupervised learning to train the network so that it has good generalization ability for a wide range of system and structure parameter values.The generated network FreeformNet enables fast generation(less than 0.003 s per system)of multiple-solution systems after we input the design requirements,including the system and structure parameters.We can filter and sort solutions based on a given criterion and use them as good starting points for quick final optimization(several seconds for systems with small or moderate field-of-view in general).The proposed framework presents a revolutionary approach to the lens design of freeform or generalized imaging systems,thus significantly reducing the time and effort expended on optical design.

Aquaporin-4-IgG-seropositive neuromyelitis optica spectrum disorders:progress of experimental models based on disease pathogenesis

Neuromyelitis optica spectrum disorders are neuroinflammatory demyelinating disorders that lead to permanent visual loss and motor dysfunction.To date,no effective treatment exists as the exact causative mechanism remains unknown.Therefore,experimental models of neuromyelitis optica spectrum disorders are essential for exploring its pathogenesis and in screening for therapeutic targets.Since most patients with neuromyelitis optica spectrum disorders are seropositive for IgG autoantibodies against aquaporin-4,which is highly expressed on the membrane of astrocyte endfeet,most current experimental models are based on aquaporin-4-IgG that initially targets astrocytes.These experimental models have successfully simulated many pathological features of neuromyelitis optica spectrum disorders,such as aquaporin-4 loss,astrocytopathy,granulocyte and macrophage infiltration,complement activation,demyelination,and neuronal loss;however,they do not fully capture the pathological process of human neuromyelitis optica spectrum disorders.In this review,we summarize the currently known pathogenic mechanisms and the development of associated experimental models in vitro,ex vivo,and in vivo for neuromyelitis optica spectrum disorders,suggest potential pathogenic mechanisms for further investigation,and provide guidance on experimental model choices.In addition,this review summarizes the latest information on pathologies and therapies for neuromyelitis optica spectrum disorders based on experimental models of aquaporin-4-IgG-seropositive neuromyelitis optica spectrum disorders,offering further therapeutic targets and a theoretical basis for clinical trials.

Fekete and Szego problem for a subclass of quasi-convex mappings in several complex variables

让 K 是在联合起来的磁盘的规范的凸的函数的熟悉的类。Keogh 和 Merkes 证明了著名结果是那最大 ? fK|a3&minus;&lambda;a22|&le;max ?{ 1/3 &comma;|&lambda;&minus;1|}&comma;&lambda;? ，并且估计为每 &lambda; 是锋利的。我们为在一个复杂 Banach 空格或在联合起来的 polydisk 上在联合起来的球定义在的类型 B 的伪凸的 mappings 的一个子类调查相应问题 ? n。这些结果的证明使用一些限制假设，在一建筑群的情况中，变量它自动地满足。