Mitre Corporation

About: Mitre Corporation is a company organization based out in Bedford, Massachusetts, United States. It is known for research contribution in the topics: Air traffic control & National Airspace System. The organization has 4884 authors who have published 6053 publications receiving 124808 citations. The organization is also known as: Mitre & MITRE.

Embedded Training for Complex Information Systems

Abstract: One solution to providing affordable operator training in the workplace is to augment applications with intelligent embedded training systems. Intelligent embedded training is highly interactive: trainees practice problem-solving tasks on the prime application with guidance and feedback from the training system. We group the necessary assistance mechanisms into three layers: (1) an application interface layer, (2) an action interpretation layer, and (3) a training services layer. We discuss these layers, their interactions, and our prototype implementation of each one.

Symbol-balanced quaternionic periodicity transform for latent pattern detection in DNA sequences

Abstract: A new approach towards computing the periodicity transform of DNA sequences is proposed. The approach is based on the mapping of DNA symbols to pure quaternions. The resulting quaternionic periodicity transform outperforms the previously proposed complex periodicity transform due to enhanced, symbol-balanced sensitivity to DNA patterns. The theoretical finding is supported by a performance comparison of the two transforms and by an application example.

Self-monitoring fiber optic link

Abstract: The self-monitoring link utilizes a GRIN lens/blazed grating combination to multiplex an optical time domain reflectometry (OTDR) signal with data signals on a fiber optic communication link. An initial average OTDR reference signature for the OTDR signal on the link is determined and is compared with a continuously determined average OTDR signature. The reference signature and the continuously determined signature are compared and a warning or alarm signal is generated when the continuously determined signature differs from the reference signature by a preselectable limit. A microprocessor is provided to adjust the preselectable limit in response to the communication link operational parameters.

SHORT COMMUNICATION: Phenobarbital selectively promotes initiated cells with reduced TGFβ receptor levels

Abstract: Phenobarbital (PB) is a potent tumor promoter in rodentliver. In this study we investigated whether PB selectivelypromotes a population of initiated cells with reduced levelsof transforming growth factor-P (TGFP) receptors types I,II and III. Liver tumors were induced in male Fischer F344rats by diethylnitrosamine (DEN). Following inductionthe animals were divided into PB-treated (DEN/PB) anduntreated groups (DEN). After 3 months of treatment halfof the PB-treated rats were removed from PB for the finalmonth (DEN/PB/OFF). At 4 months, the livers from ratsin the three treatment groups were removed, tumors excisedand frozen with matched surrounding normal tissue. ThemRNA levels for the TGFp receptors types I-HI weresignificantly decreased in tumor tissue from DEN/PB ratswhen compared with surrounding normal liver tissue ortumors from age-matched untreated controls. In tumorsfrom DEN/PB/OFF rats the TGFp receptor types I-mwere also significantly reduced compared with controls andnot different to tumors from DEN/PB rats. There was nodifference in the mRNA levels for the TGFP receptors intumors from rats exposed to DEN alone, when comparedwith the surrounding normal tissue. These results demon-strate that PB selectively promotes initiated cells withreduced levels of TGFP types I-HI receptors and suggestsa mechanistic role for TGFp in PB-induced liver tumorpromotion.Approximately 60% of the chemicals determined by theNational Toxicology Program to be carcinogenic in rats andmice give rise to liver tumors. Some of these carcinogens,however, are either only weakly genotoxic or have been foundto cause no detectable genetic damage. Rather, they appear tofunction as tumor promoting agents. These agents includechemicals to which humans are exposed, e.g. contraceptivesteroids (1,2), tamoxifen (3), benzodiazepine compounds (4),dioxin (5), and phenobarbital (PB*) (6). Although there is nodefinitive mechanism for the carcinogenic activity of thesediverse agents, one hypothesis involves reduced reponsivenessto negative growth signals, especially the potent mitoinhibitortransforming growth factor-P (TGFP) (7).In mammals TGFP exists as three highly homologousisoforms, TGFpi, TGFP2 and TGFP3 (8). These structurally