Terahertz imaging with sub-wavelength resolution by femtosecond laser filament in air

Terahertz (THz) imaging provides cutting edge technique in biology, medical sciences and non-destructive evaluation. However, due to the long wavelength of the THz wave, the obtained resolution of THz imaging is normally a few hundred microns and is much lower than that of the traditional optical imaging. We introduce a sub-wavelength resolution THz imaging technique which uses the THz radiation generated by a femtosecond laser filament in air as the probe. This method is based on the fact that the femtosecond laser filament forms a waveguide for the THz wave in air. The diameter of the THz beam, which propagates inside the filament, varies from 20 {\mu}m to 50 {\mu}m, which is significantly smaller than the wavelength of the THz wave. Using this highly spatially confined THz beam as the probe, THz imaging with resolution as high as 20 {\mu}m (~{\lambda}/38) can be realized.Comment: 10 pages, 7 figure

Empathetic Response Generation with State Management

A good empathetic dialogue system should first track and understand a user's emotion and then reply with an appropriate emotion. However, current approaches to this task either focus on improving the understanding of users' emotion or on proposing better responding strategies, and very few works consider both at the same time. Our work attempts to fill this vacancy. Inspired by task-oriented dialogue systems, we propose a novel empathetic response generation model with emotion-aware dialogue management. The emotion-aware dialogue management contains two parts: (1) Emotion state tracking maintains the current emotion state of the user and (2) Empathetic dialogue policy selection predicts a target emotion and a user's intent based on the results of the emotion state tracking. The predicted information is then used to guide the generation of responses. Experimental results show that dynamically managing different information can help the model generate more empathetic responses compared with several baselines under both automatic and human evaluations

Expression of Robo4 in the fibrovascular membranes from patients with proliferative diabetic retinopathy and its role in RF/6A and RPE cells

Purpose: Robo4, a member of the roundabout (Robo) family, acts as a neuronal guidance receptor and plays some role in vasculogenesis and angiogenesis. This study investigated the effect of Robo4 on the formation of fibrovascular membranes (FVMs) from patients with proliferative diabetic retinopathy and its roles in choroid-retina endothelial (RF/6A) and human retinal pigment epithelial (RPE) cells. Methods: RT-PCR and immunohistochemistry were used to determine the levels of mRNA and the presence and distribution of Robo4 in FVMs. Small interfering RNA (siRNA) technology was used to knock down Robo4 expression and to study its effects on RF/6A and RPE cells in vitro. Cell proliferation, migration, spreading, cycling, and apoptosis were assessed with MTT assay, Boyden chamber assay, immunocytochemistry, and flow cytometry. Tube formation by RF/6A on Matrigel was also analyzed. Results: The level of Robo4 mRNA was high in FVMs. Robo4 was expressed in the vessels and fibrous-like tissue co-immunostained for CD31 and GFAP, respectively. Robo4 siRNA knockdown inhibited cell proliferation and migration. Tube formation by RF/6A cells was also disturbed. Under hypoxic conditions, more apoptotic cells were evident among the knockdown cells than among the control cells (p < 0.01). Conclusions: Robo4 may play a role in the formation of FVMs. Silencing the expression of Robo4 in RF/6A and RPE cells inhibited their proliferation and reduced their tolerance of hypoxic conditions, suggesting physiologic functions of Robo4 in the cells of the retina.http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000267136400001&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=8e1609b174ce4e31116a60747a720701Biochemistry & Molecular BiologyOphthalmologySCI(E)PubMed15ARTICLE112-131057-10691

Impaired Coenzyme A metabolism affects histone and tubulin acetylation in Drosophila and human cell models of pantothenate kinase associated neurodegeneration

Pantothenate kinase-associated neurodegeneration (PKAN is a neurodegenerative disease with unresolved pathophysiology. Previously, we observed reduced Coenzyme A levels in a Drosophila model for PKAN. Coenzyme A is required for acetyl-Coenzyme A synthesis and acyl groups from the latter are transferred to lysine residues of proteins, in a reaction regulated by acetyltransferases. The tight balance between acetyltransferases and their antagonistic counterparts histone deacetylases is a well-known determining factor for the acetylation status of proteins. However, the influence of Coenzyme A levels on protein acetylation is unknown. Here we investigate whether decreased levels of the central metabolite Coenzyme A induce alterations in protein acetylation and whether this correlates with specific phenotypes of PKAN models. We show that in various organisms proper Coenzyme A metabolism is required for maintenance of histone- and tubulin acetylation, and decreased acetylation of these proteins is associated with an impaired DNA damage response, decreased locomotor function and decreased survival. Decreased protein acetylation and the concurrent phenotypes are partly rescued by pantethine and HDAC inhibitors, suggesting possible directions for future PKAN therapy development

Restructuring “Asian Film”: Maoist Revolutionary Worldviews, Film Festivals and the Cold War in Asia

AAS Conference pape

Translation and Internationalism

Mao's Little red book: a global history76-9

Little Teachers: Children's Drama, Traveling, and Ruptured Childhoods in 1930s and 1940s China

10.1080/15215385.2016.1155288Twentieth-Century China412180-20

PDCD5 Interacts with Tip60 and Functions as a Cooperator in Acetyltransferase Activity and DNA Damage-Induced Apoptosis

Tip60 is a histone acetyltransferase (HAT) involved in the acetyltransferase activity and the cellular response to DNA damage. Here, we show that programmed cell death 5 (PDCD5), a human apoptosis-related protein, binds to Tip60 and enhances the stability of Tip60 protein in unstressed conditions. The binding amount of PDCD5 and Tip60 is significantly increased after UV irradiation. Further, PDCD5 enhances HAT activity of Tip60 and Tip60-dependent histone acetylation in both basal and UV-induced levels. We also find that PDCD5 increases Tip60-dependent K120 acetylation of p53 and participates in the p53-dependent expression of apoptosis-related genes, such as Bax. Moreover, we demonstrate the biological significance of the PDCD5-Tip60 interaction; that is, they function in cooperation to accelerate DNA damage-induced apoptosis and knockdown of PDCD5 or Tip60 impairs their apoptosis-accelerating activity, mutually. Consistent with this, PDCD5 levels increase significantly on DNA damage in U2OS cells, as does Tip60. Together, our findings indicate that PDCD5 may play a dual role in the Tip60 pathway. Specifically, under normal growth conditions, PDCD5 contributes to maintaining a basal pool of Tip60 and its HAT activity. After DNA damage, PDCD5 functions as a Tip60 coactivator to promote apoptosis