160 research outputs found

    The Cognitive Load of Observation Tasks in 3D Video is Lower Than That in 2D Video

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    We are exposed to more and more 3D videos, some for entertainment and some for scientific research. Some experiments using 3D video as a stimulus focus only on its visual effect. We studied the cognitive difference between 3D and 2D videos by analyzing EEG. This research adopts a 2 x 4 experimental design, including 2D and 3D versions of 4 video scenes. These four video scenes can be classified into two simple task scenes and two complex task scenes. The simple task scenario and the complex task scenario each contain a video with violent content changes and a calm video. Subjects need to watch eight videos. We recorded the EEG information of the subjects and analyzed the power of alpha and theta oscillations. On this basis, we calculated the cognitive load index (CLI), which can be used as an indicator of cognitive load. The results showed that 3D videos that required subjects to perform simple tasks brought higher cognitive load to most subjects. When the video contains complex tasks, the cognitive load of subjects does not show similar regularity. Specifically, only half of the people had higher cognitive load when watching the 3D version of the video than when watching the 2D version. In addition, the cognitive load level of subjects showed significant individual differencesComment: 7 pages, 18 figure

    Diversity-Oriented Synthesis for Novel, Selective and Drug-like Inhibitors for a Phosphatase from Mycobacterium Tuberculosis

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    Mycobacterium protein tyrosine phosphatase B (mPTPB) is a potential drug target of Tuberculosis (TB). Small molecule inhibitors of mPTPB could be a treatment to overcome emerging TB drug resistance. Using a Diversity-Oriented Synthesis (DOS) strategy, we successfully developed a salicylic acid based and drug-like mPTPB inhibitor with an IC50 of 2 μM and >20-fold specificity over many human PTPs, making it an excellent lead molecule for anti-TB drug discovery. In addition, DOS generated bicyclic salicylic acids are also promising starting points for acquiring inhibitors targeting other PTPs

    Etching kinetics and surface roughening of polysilicon and dielectric materials in inductively coupled plasma beams

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    Thesis (Ph. D.)--Massachusetts Institute of Technology, Dept. of Chemical Engineering, 2007.Includes bibliographical references.Plasma etching processes often roughen the feature sidewalls forming anisotropic striations. A clear understanding of the origin and control of sidewall roughening is extremely desirable, particularly at the gate level where variations in line width can adversely impact the electrical performance of the device. In addition, at the back end, feature sidewall roughness of the dielectric materials might degrade the resolution of contacts, interfere with the deposition of conformal liner materials, and make the process integration challengeable. In an inductively coupled plasma apparatus, the etching behavior on real feature sidewalls was simulated by etching blank films at grazing ion bombardment angles. The angular etching yields of polysilicon and dielectric materials in Ar, C12/Ar, and C4F8/Ar plasma beams were studied as a function of ion bombardment energy, ion bombardment angle, etching time, plasma pressure, and plasma composition. Interestingly, the effective neutral-to-ion flux ratio was the primary factor influencing the etching yield. A typical sputtering angular yield curve, with a peak around 600 off-normal angle, was formed at non-saturated etching regime, while an ion-enhanced-etching angular yield curve peaked around 650 was observed in the saturated etching regime.(cont.) In Ar plasma, various films remained smooth after etching at normal angle but became rougher at grazing angles. Specifically, the striation structure formed at grazing angles could be either parallel or transverse to the beam impingement direction. Encouragingly, the sputtering caused roughening at different off-normal angles could be qualitatively explained by the corresponding angular dependent etching yield curve. In fluorocarbon plasmas, the roughening of thermal silicon dioxide and low-k coral films at grazing ion bombardment angles depended on both the etching kinetics and the etching chemistry. In particular, the surface roughened when the etching process was physical-sputtering like (at low neutral-to-ion flux ratios), even though the polymer deposition effect was trivial; when the etching kinetics was dominated by ion-enhanced etching (at high neutral-to-ion flux ratios), the roughening was mainly caused by the local polymer deposition effects. Moreover, surfaces could be etched without roughening at intermediate neutral-to-ion flux ratios and/or with the addition of oxygen to the discharge. The oxygen addition broadened the region over which etching without roughening can be performed.(cont.) Additionally, the local-polymer-deposition effect can be used to explain the surface roughening of porous low-k films in fluorocarbon plasmas. Last, it was shown that RMS roughness is not adequate to represent the surface roughness on etched surfaces, especially when anisotropic striations exist. Instead, statistical methods such as the power spectral density and geostatistical analysis are capable of measuring the surface roughening in both vertical and lateral dimensions. In this way, the spatial variation of the streaks formed during plasma etching can be characterized quantitatively.by Yunpeng Yin.Ph.D

    Role of phosphatase of regenerating liver 1 (PRL1) in spermatogenesis

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    The PRL phosphatases are oncogenic when overexpressed but their in vivo biological function is less well understood. Previous gene deletion study revealed a role for PRL2 in spermatogenesis. We report here the first knockout mice lacking PRL1, the most related homolog of PRL2. We found that loss of PRL1 does not affect spermatogenesis and reproductive ability of male mice, likely due to functional compensation by the relatively higher expression of PRL2 in the testes. However, PRL1-/-/PRL2+/- male mice show testicular atrophy phenotype similar to PRL2-/- mice. More strikingly, deletion of one PRL1 allele in PRL2-/- male mice causes complete infertility. Mechanistically, the total level of PRL1 and PRL2 is negatively correlated with the PTEN protein level in the testis and PRL1+/-/PRL2-/- mice have the highest level of PTEN, leading to attenuated Akt activation and increased germ cell apoptosis, effectively halting spermatozoa production. These results provide the first evidence that in addition to PRL2, PRL1 is also required for spermatogenesis by downregulating PTEN and promoting Akt signaling. The ability of the PRLs to suppress PTEN expression underscores the biochemical basis for their oncogenic potential

    Novel anticancer agents based on targeting the trimer interface of the PRL phosphatase

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    PRL oncoproteins are phosphatases overexpressed in numerous types of human cancer. Elevated levels of PRL associate with metastasis and poor clinical outcomes. In principle, PRL phosphatases offer appealing therapeutic targets, but they remain underexplored due to the lack of specific chemical probes. In this study, we address this issue by exploiting a unique property of PRL phosphatases, namely, that they may function as homotrimers. Starting from a sequential structure-based virtual screening and medicinal chemistry strategy, we identified Cmpd-43 and several analogs which disrupt PRL1 trimerization. Biochemical and structural analyses demonstrate that Cmpd-43 and its close analogs directly bind the PRL1 trimer interface and obstruct PRL1 trimerization. Cmpd-43 also specifically blocks the PRL1-induced cell proliferation and migration through attenuation of both ERK1/2 and Akt activity. Importantly, Cmpd-43 exerted potent anticancer activity both in vitro and in vivo in a murine xenograft model of melanoma. Our results validate a trimerization-dependent signaling mechanism for PRL and offer proof-of-concept for trimerization inhibitors as candidate therapeutics to treat PRL-driven cancer

    SHP2 phosphatase as a novel therapeutic target for melanoma treatment

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    Melanoma ranks among the most aggressive and deadly human cancers. Although a number of targeted therapies are available, they are effective only in a subset of patients and the emergence of drug resistance often reduces durable responses. Thus there is an urgent need to identify new therapeutic targets and develop more potent pharmacological agents for melanoma treatment. Herein we report that SHP2 levels are frequently elevated in melanoma, and high SHP2 expression is significantly associated with more metastatic phenotype and poorer prognosis. We show that SHP2 promotes melanoma cell viability, motility, and anchorage-independent growth, through activation of both ERK1/2 and AKT signaling pathways. We demonstrate that SHP2 inhibitor 11a-1 effectively blocks SHP2-mediated ERK1/2 and AKT activation and attenuates melanoma cell viability, migration and colony formation. Most importantly, SHP2 inhibitor 11a-1 suppresses xenografted melanoma tumor growth, as a result of reduced tumor cell proliferation and enhanced tumor cell apoptosis. Taken together, our data reveal SHP2 as a novel target for melanoma and suggest SHP2 inhibitors as potential novel therapeutic agents for melanoma treatment
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