Workshops of the Sixth International Brain–Computer Interface Meeting: brain–computer interfaces past, present, and future

Brain–computer interfaces (BCI) (also referred to as brain–machine interfaces; BMI) are, by definition, an interface between the human brain and a technological application. Brain activity for interpretation by the BCI can be acquired with either invasive or non-invasive methods. The key point is that the signals that are interpreted come directly from the brain, bypassing sensorimotor output channels that may or may not have impaired function. This paper provides a concise glimpse of the breadth of BCI research and development topics covered by the workshops of the 6th International Brain–Computer Interface Meeting

A preliminary survey on the perception of marketability of brain-computer interfaces and initial development of a repository of BCI companies

The marketability of BCI applications may greatly influence the decisions of goverments, the industry and academia. In this paper we first explored with a survey when respondents (N = 145), who were present at the 4th International BCI Meeting, expect that different BCI applications will become commercially available. Second, we surveyed how well existing BCI companies are known to respondents. Third, we compared the findings with our own preliminary overview of the marketability of BCIs and our repository of 28 companies. Respondents were optimistic about the marketability of BCIs for healthy users and users who need assistive technology (AT), but 72.4% of the respondents was unaware that companies already exist which market BCI's. Based on a preliminary market overview we cautiously suggest that optimism in relation to applications for healthy users is more appropriate than in relation to BCI-based AT. In future we plan surveys among a broader range of stakeholders and more profound analyses of the market

TLR9 re-expression in cancer cells extends the S-phase and stabilizes p16(INK4a) protein expression

International audienceToll-like receptor 9 (TLR9) recognizes bacterial, viral or cell damage-associated DNA, which initiates innate immune responses. We have previously shown that TLR9 expression is downregulated in several viral induced cancers including HPV16-induced cervical neoplasia. Findings supported that downregulation of TLR9 expression is involved in loss of anti-viral innate immunity allowing an efficient viral replication. Here we investigated the role of TLR9 in altering the growth of transformed epithelial cells. Re-introducing TLR9 under the control of an exogenous promoter in cervical or head and neck cancer patient-derived cells reduced cell proliferation, colony formation and prevented independent growth of cells under soft agar. Neither TLR3, 7, nor the TLR adapter protein MyD88 expression had any effect on cell proliferation, indicating that TLR9 has a unique role in controlling cell growth. The reduction of cell growth was not due to apoptosis or necrosis, yet we observed that cells expressing TLR9 were slower in entering the S-phase of the cell cycle. Microarray-based gene expression profiling analysis highlighted a strong interferon (IFN) signature in TLR9-expressing head and neck cancer cells, with an increase in IFN-type I and IL-29 expression (IFN-type III), yet neither IFN-type I nor IL-29 production was responsible for the block in cell growth. We observed that the protein half-life of p16(INK4a) was increased in TLR9-expressing cells. Taken together, these data show for the first time that TLR9 affects the cell cycle by regulating p16(INK4a) post-translational modifications and highlights the role of TLR9 in the events that lead to carcinogenesi