AudioFunctions.web: Multimodal Exploration of Mathematical Function Graphs

We present AudioFunctions.web, a web app that uses sonifcation, earcons and speech synthesis to enable blind people to explore mathematical function graphs. The system is designed for personalized access through different interfaces (touchscreen, keyboard, touchpad and mouse) on both mobile and traditional devices, in order to better adapt to different user abilities and preferences. It is also publicly available as a web service and can be directly accessed from the teaching material through a hypertext link. An experimental evaluation with 13 visually impaired participants highlights that, while the usability of all the presented interaction modalities is high, users with different abilities prefer different interfaces to interact with the system. It is also shown that users with higher level of mathematical education are capable of better adapting to interaction modalities considered more diffcult by others

Axessibility: a LaTeX Package for Mathematical Formulae Accessibility in PDF Documents

Accessing mathematical formulae within digital documents is challenging for blind people. In particular, document formats designed for printing, such as PDF, structure math content for visual access only. While accessibility features exist to present PDF content non-visually, formulae support is limited to providing replacement text that can be read by a screen reader or displayed on a braille bar. However, the operation of inserting replacement text is left to document authors, who rarely provide such content. Furthermore, at best, description of the formulae are provided. Thus, conveying detailed understanding of complex formulae is nearly impossible. In this contribution we report our ongoing research on Axessibility, a LATEX package framework that automates the process of making mathematical formulae accessible by providing the formulae LATEX code as PDF replacement text. Axessibility is coupled with external scripts to automate its integration in existing documents, expand user shorthand macros to standard LATEX representation, and custom screen reader dictionaries that improve formulae reading on screen readers

Dickkopf-related protein 1 (Dkk1) regulates the accumulation and function of myeloid derived suppressor cells in cancer

Tumor–stroma interactions contribute to tumorigenesis. Tumor cells can educate the stroma at primary and distant sites to facilitate the recruitment of heterogeneous populations of immature myeloid cells, known as myeloid-derived suppressor cells (MDSCs). MDSCs suppress T cell responses and promote tumor proliferation. One outstanding question is how the local and distant stroma modulate MDSCs during tumor progression. Down-regulation of β-catenin is critical for MDSC accumulation and immune suppressive functions in mice and humans. Here, we demonstrate that stroma-derived Dickkopf-1 (Dkk1) targets β-catenin in MDSCs, thus exerting immune suppressive effects during tumor progression. Mice bearing extraskeletal tumors show significantly elevated levels of Dkk1 in bone microenvironment relative to tumor site. Strikingly, Dkk1 neutralization decreases tumor growth and MDSC numbers by rescuing β-catenin in these cells and restores T cell recruitment at the tumor site. Recombinant Dkk1 suppresses β-catenin target genes in MDSCs from mice and humans and anti-Dkk1 loses its antitumor effects in mice lacking β-catenin in myeloid cells or after depletion of MDSCs, demonstrating that Dkk1 directly targets MDSCs. Furthermore, we find a correlation between CD15(+) myeloid cells and Dkk1 in pancreatic cancer patients. We establish a novel immunomodulatory role for Dkk1 in regulating tumor-induced immune suppression via targeting β-catenin in MDSCs

Проблеми інноваційного розвитку підприємств вугільної галузі України

Метою статті є визначення проблем інноваційного розвитку вугільної галузі та напрями його забезпечення шляхом упровадження інновацій

Stromal senescence establishes an immunosuppressive microenvironment that drives tumorigenesis

Age is a significant risk factor for the development of cancer. However, the mechanisms that drive age-related increases in cancer remain poorly understood. To determine if senescent stromal cells influence tumorigenesis, we develop a mouse model that mimics the aged skin microenvironment. Using this model, here we find that senescent stromal cells are sufficient to drive localized increases in suppressive myeloid cells that contributed to tumour promotion. Further, we find that the stromal-derived senescence-associated secretory phenotype factor interleukin-6 orchestrates both increases in suppressive myeloid cells and their ability to inhibit anti-tumour T-cell responses. Significantly, in aged, cancer-free individuals, we find similar increases in immune cells that also localize near senescent stromal cells. This work provides evidence that the accumulation of senescent stromal cells is sufficient to establish a tumour-permissive, chronic inflammatory microenvironment that can shelter incipient tumour cells, thus allowing them to proliferate and progress unabated by the immune system