Transformation media that turn a narrow slit into a large window

Based on the transformation media theory, the authors propose a way to replace a wide window with a narrow slit filled with designed metamaterial to achieve the same transmittance as the one of the window. Numerical simulations for a two dimensional case are given to illustrate the ideas and the performance of the design.Comment: 10 pages, 3 figure

Directory of English/Chinese Names of Scholars in Chinese Studies - 海外中国研究学者名录（英中对照）

The Directory of English/Chinese Names of Scholars in Chinese Studies was a by-product of the "Chinese Studies in North America - Research and Resources" project. It provides both the English and the Chinese names of scholars involved in Chinese Studies mainly in North America. The Chinese names for western scholars resulted from an extensive in the relevant literature and on the internet at appropriate sites to find and authenticate the Chinese names used by these scholars. Where we could not find the Chinese name adopted by a scholar, we have transliterated their name into Chinese characters using the standard reference book 英语姓名译名手册. It is hoped that this directory will be useful for people needing to search for the Chinese names used by western scholars, or for the standard transliterations of their names into Chinese characters. Corrections of inaccurate information and addition of new names of Chinese Studies scholars worldwide are welcome. For corrections, comments and updates, please send emails to Haihui Zhang (Librarian for Chinese studies at East Asian Library, University Library System at University of Pittsburgh) at [email protected]

Removal of Hsf4 leads to cataract development in mice through down-regulation of γS-crystallin and Bfsp expression

<p>Abstract</p> <p>Background</p> <p>Heat-shock transcription factor 4 (HSF4) mutations are associated with autosomal dominant lamellar cataract and Marner cataract. Disruptions of the <it>Hsf4 </it>gene cause lens defects in mice, indicating a requirement for HSF4 in fiber cell differentiation during lens development. However, neither the relationship between HSF4 and crystallins nor the detailed mechanism of maintenance of lens transparency by HSF4 is fully understood.</p> <p>Results</p> <p>In an attempt to determine how the underlying biomedical and physiological mechanisms resulting from loss of HSF4 contribute to cataract formation, we generated an <it>Hsf4 </it>knockout mouse model. We showed that the <it>Hsf4 </it>knockout mouse (<it>Hsf4</it>^-/-) partially mimics the human cataract caused by HSF4 mutations. Q-PCR analysis revealed down-regulation of several cataract-relevant genes, including <it>γS-crystallin (Crygs) </it>and lens-specific beaded filament proteins 1 and 2 (<it>Bfsp1 </it>and <it>Bfsp2</it>), in the lens of the <it>Hsf4</it>^-/-mouse. Transcription activity analysis using the dual-luciferase system suggested that these cataract-relevant genes are the direct downstream targets of HSF4. The effect of HSF4 on <it>γS-crystallin </it>is exemplified by the cataractogenesis seen in the <it>Hsf4</it>^-/-,<it>rncat </it>intercross. The 2D electrophoretic analysis of whole-lens lysates revealed a different expression pattern in 8-week-old <it>Hsf4</it>^-/-mice compared with their wild-type counterparts, including the loss of some αA-crystallin modifications and reduced expression of γ-crystallin proteins.</p> <p>Conclusion</p> <p>Our results indicate that HSF4 is sufficiently important to lens development and disruption of the <it>Hsf4 </it>gene leads to cataracts via at least three pathways: 1) down-regulation of <it>γ-crystallin</it>, particularly <it>γS-crystallin</it>; 2) decreased lens beaded filament expression; and 3) loss of post-translational modification of αA-crystallin.</p

VITAL: VIsual Tracking via Adversarial Learning

The tracking-by-detection framework consists of two stages, i.e., drawing samples around the target object in the first stage and classifying each sample as the target object or as background in the second stage. The performance of existing trackers using deep classification networks is limited by two aspects. First, the positive samples in each frame are highly spatially overlapped, and they fail to capture rich appearance variations. Second, there exists extreme class imbalance between positive and negative samples. This paper presents the VITAL algorithm to address these two problems via adversarial learning. To augment positive samples, we use a generative network to randomly generate masks, which are applied to adaptively dropout input features to capture a variety of appearance changes. With the use of adversarial learning, our network identifies the mask that maintains the most robust features of the target objects over a long temporal span. In addition, to handle the issue of class imbalance, we propose a high-order cost sensitive loss to decrease the effect of easy negative samples to facilitate training the classification network. Extensive experiments on benchmark datasets demonstrate that the proposed tracker performs favorably against state-of-the-art approaches.Comment: Spotlight in CVPR 201

Genome Editing of Pik3cd Impedes Abnormal Retinal Angiogenesis

Abnormal angiogenesis is associated with myriad human diseases including proliferative diabetic retinopathy. Signaling transduction via phosphoinositide 3-kinases (PI3Ks) plays a critical role in angiogenesis. Herein, we showed that p110δ, the catalytic subunit of PI3Kδ, was highly expressed in pathological retinal vascular endothelial cells (ECs) in a mouse model of oxygen-induced retinopathy (OIR) and in fibrovascular membranes from patients with proliferative diabetic retinopathy. To explore novel intervention with PI3Kδ expression, we developed a recombinant dual adeno-associated viral (rAAV) system for delivering CRISPR/Cas9 in which Streptococcus pyogenes (Sp) Cas9 expression was driven by an endothelial specific promoter of intercellular adhesion molecule 2 (pICAM2) to edit genomic Pik3cd, the gene encoding p110δ. We then demonstrated that infection of cultured mouse vascular endothelial cells with the dual rAAV1s of rAAV1-pICAM2-SpCas9 and rAAV1-SpGuide targeting genomic Pik3cd resulted in 80% DNA insertion/deletion in the locus of genomic Pik3cd and 70% depletion of p110δ expression. Furthermore, we showed that in the mouse model of OIR editing retinal Pik3cd with the dual rAAV1s resulted in not only a significant decrease in p110δ expression, and Akt activation, but also a dramatic reduction in pathological retinal angiogenesis. These findings reveal that Pik3cd editing is a novel approach to treating abnormal retinal angiogenesis

Correction to: Genome Editing of Pik3cd Impedes Abnormal Retinal Angiogenesis, by Wu et al. Hum Gene Ther 2023;34(1-2):30-41; doi: 10.1089/hum.2022.079

In the January 2023 issue of Human Gene Therapy (vol. 34, no. 1-2; 30–41), the article titled Genome Editing of Pik3cd Impedes Abnormal Retinal Angiogenesis, by Wu et al. requires correction. The author byline originally appeared with the 13th author's name incorrectly published as GuomingZhao Wenyi Wu,1,2,3 Gaoen Ma,4 Hui Qi,5 Lijun Dong,5 Fang Chen,6 Yun Wang,5 Xingxing Mao,5 Xiaoqing Guo,2,3 Jing Cui,7 Joanne Aiko Matsubara,7 Bart Vanhaesebroeck,8 Xiaohe Yan,5Guoming Zhao,5 Shaochong Zhang,5,* and Hetian Lei 5,* The correct spelling of the author's name is GuomingZhang The online version of the article has been corrected to reflect this. The authors apologize for the error