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RISS 인기검색어
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- 저자 : Weisenberger, (검색결과 3 건)
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Human sensory feedback research in the armstrong laboratory
Weisenberger, Janet M. Ergonomics Society of Korea 1997 大韓人間工學會誌 Vol.16 No.2
The Human Sensory Feedback Laboratory, park of the Armstrong Laboratory at Wright-Patterson Air Force Base, Ohio, is involved in the development and evaluation of systems that provide sensory feedback to the human operator in telerobotic and virtual environment applications. Specific projects underway in the laboratory are primarily concerned with the information provided by force and vibrotactile feedback to the operator in dextrous manipulation tasks. Four specific research projects are described in the present report. These include : 1) experiments evaluating a 30-element fingertip display, which employs a titanium-nickel shape memory alloy actuator design to provide vibrotactile feedback about object shape and surface texture ; 2) of a fingertip force-feedback display for 3-dimensional information about object shape and suface texture ; 3) use of a force- feedback joystic to provide "force tunnel" information in pilot pursuit tracking tasks ; and 4) evaluations of a 7 degree-of-freedom exoskeleton used to control a robotic arm. Both basic and applied research questions are discussed.
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Genetic and Epigenetic Alterations in Bladder Cancer
Hong-Tao Li,Christopher E. Duymich,Daniel J. Weisenberger,Gangning Liang 대한배뇨장애요실금학회 2016 International Neurourology Journal Vol.20 No.S1
Bladder cancer is one of the most common cancers worldwide, with a high rate of recurrence and poor outcomes as a result of relapse. Bladder cancer patients require lifelong invasive monitoring and treatment, making bladder cancer one of the most expensive malignancies. Lines of evidence increasingly point to distinct genetic and epigenetic alteration patterns in bladder cancer, even between the different stages and grades of disease. In addition, genetic and epigenetic alterations have been demonstrated to play important roles during bladder tumorigenesis. This review will focus on bladder cancer-associated genomic and epigenomic alterations, which are common in bladder cancer and provide potential diagnostic markers and therapeutic targets for bladder cancer treatment.
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Kang, Gyeong Hoon,Lee, Sun,Cho, Nam-Yun,Gandamihardja, Tasha,Long, Tiffany I,Weisenberger, Daniel J,Campan, Mihaela,Laird, Peter W United States and Canadian Academy of Pathology [e 2008 Laboratory investigation Vol.88 No.2
<P>Transcriptional silencing by CpG island hypermethylation is a potential mechanism for the inactivation of tumor-related genes. Virtually, all types of human cancers show CpG island hypermethylation, and gastric carcinoma (GC) is one of the tumors with a high frequency of aberrant CpG island hypermethylation. In this study, we prescreened DNA methylation of 170 CpG island loci in a training set of 8 paired GC and GC-associated non-neoplastic mucosae (GCN) using MethyLight technology and selected 27 DNA methylation markers showing higher methylation frequency or level in GC than in GCN. These markers were then analyzed in a tester set of 25 paired GC and GCN and 27 chronic gastritis (CG) from non-cancer patients to generate their DNA methylation profiles. We identified 17 novel methylation markers in GC, including SFRP4, SEZ6L, TWIST1, BCL2, KL, TERT, SCGB3A1, IGF2, GRIN2B, SFRP5, DLEC1, HOXA1, CYP1B1, SMAD9, MT1G, NR3C1, and HOXA10. Of the 27 selected CpG island loci, 23 were methylated in GC, GCN, and CG and the remainder four loci (DLEC1, CHFR, CYP1B1, and NR3C1) were only methylated in GC. We found that the number of methylated loci was significantly higher in GC than in GCN or CG and that Helicobacter pylori infection was strongly associated with aberrant CpG island hypermethylation in CG. Hypermethylation was more prevalent in Epstein-Barr virus (EBV)-positive GC than in EBV-negative GC and in diffuse-type GC than in intestinal-type GC. Through our large-scale screening of 170 CpG island loci, we found 17 new DNA methylation markers of GC, which may serve as useful markers that may identify a distinct subset of GC.</P>
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