Auditory Measures for the Next Billion Users.

A range of new technologies have the potential to help people, whether traditionally considered hearing impaired or not. These technologies include more sophisticated personal sound amplification products, as well as real-time speech enhancement and speech recognition. They can improve user's communication abilities, but these new approaches require new ways to describe their success and allow engineers to optimize their properties. Speech recognition systems are often optimized using the word-error rate, but when the results are presented in real time, user interface issues become a lot more important than conventional measures of auditory performance. For example, there is a tradeoff between minimizing recognition time (latency) by quickly displaying results versus disturbing the user's cognitive flow by rewriting the results on the screen when the recognizer later needs to change its decisions. This article describes current, new, and future directions for helping billions of people with their hearing. These new technologies bring auditory assistance to new users, especially to those in areas of the world without access to professional medical expertise. In the short term, audio enhancement technologies in inexpensive mobile forms, devices that are quickly becoming necessary to navigate all aspects of our lives, can bring better audio signals to many people. Alternatively, current speech recognition technology may obviate the need for audio amplification or enhancement at all and could be useful for listeners with normal hearing or with hearing loss. With new and dramatically better technology based on deep neural networks, speech enhancement improves the signal to noise ratio, and audio classifiers can recognize sounds in the user's environment. Both use deep neural networks to improve a user's experiences. Longer term, auditory attention decoding is expected to allow our devices to understand where a user is directing their attention and thus allow our devices to respond better to their needs. In all these cases, the technologies turn the hearing assistance problem on its head, and thus require new ways to measure their performance.

Phorbol 12-myristate 13-acetate induces protein kinase ceta-specific proliferative response in astrocytic tumor cells.

Protein kinase C (PKC) activation has been implicated in cellular proliferation in neoplastic astrocytes. The roles for specific PKC isozymes in regulating this glial response, however, are not well understood. The aim of this study was to characterize the expression of PKC isozymes and the role of PKC-eta expression in regulating cellular proliferation in two well characterized astrocytic tumor cell lines (U-1242 MG and U-251 MG) with different properties of growth in cell culture. Both cell lines expressed an array of conventional (alpha, betaI, betaII, and gamma) and novel (theta and epsilon) PKC isozymes that can be activated by phorbol myristate acetate (PMA). Another novel PKC isozyme, PKC-eta, was only expressed by U-251 MG cells. In contrast, PKC-delta was readily detected in U-1242 MG cells but was present only at low levels in U-251 MG cells. PMA (100 nm) treatment for 24 h increased cell proliferation by over 2-fold in the U-251 MG cells, whereas it decreased the mitogenic response in the U-1242 MG cells by over 90%. When PKC-eta was stably transfected into U-1242 MG cells, PMA increased cell proliferation by 2.2-fold, similar to the response of U-251 MG cells. The cell proliferation induced by PMA in both the U-251 MG and U-1242-PKC-eta cells was blocked by the PKC inhibitor bisindolylmaleimide (0.5 micrometer) and the MEK inhibitor, PD 98059 (50 micrometer). Transient transfection of wild type U-251 with PKC-eta antisense oligonucleotide (1 micrometer) also blocked the PMA-induced increase in [(3)H]thymidine incorporation. The data demonstrate that two glioblastoma lines, with functionally distinct proliferative responses to PMA, express different novel PKC isozymes and that the differential expression of PKC-eta plays a determining role in the different proliferative capacity.