Investigating Context Awareness of Affective Computing Systems: A Critical Approach

AbstractIntelligent Human Computer Interaction systems should be affective aware and Affective Computing systems should be context aware. Positioned in the cross-section of the research areas of Interaction Context and Affective Computing current paper investigates if and how context is incorporated in automatic analysis of human affective behavior. Several related aspects are discussed ranging from modeling, acquiring and annotating issues in affectively enhanced corpora to issues related to incorporating context information in a multimodal fusion framework of affective analysis. These aspects are critically discussed in terms of the challenges they comprise while, in a wider framework, future directions of this recently active, yet mainly unexplored, research area are identified. Overall, the paper aims to both document the present status as well as comment on the evolution of the upcoming topic of Context in Affective Computing

Insulin-like growth factor-I ameliorates demyelination induced by tumor necrosis factor-α in transgenic mice

Our laboratories have reported that TNF-α causes myelin damage and apoptosis of oligodendrocytes and their precursors in vitro and in vivo. We also have reported that IGF-I can protect cultured oligodendrocytes and their precursors from TNF-α-induced damage. In this study, we investigated whether IGF-I can protect oligodendrocytes and myelination from TNF-α-induced damage in vivo by cross-breeding TNF-α transgenic (Tg) mice with IGF-I Tg mice that overexpress IGF-I exclusively in brain. At 8 weeks of age, compared to wildtype (WT) mice, the brain weights of TNF-α Tg mice were decreased by ~20%, while those of IGF-I Tg mice were increased by ~20%. The brain weights of mice that carry both TNF-α and IGF-I transgenes (TNF-α/IGF-I Tg mice) did not differ from WT mice. As judged by histochemical staining and immunostaining, myelin content in the cerebellum of TNF-α/IGF-I Tg mice was similar to that in WT mice and much more than that in TNF-α Tg mice. Consistently, western immunoblot analysis showed that myelin basic protein abundance in the cerebellum of TNF-α/IGF-I Tg mice was double that in TNF-α Tg mice. Compared to WT mice, the number of oligodendrocytes was decreased by ~36% in TNF-α Tg mice, while it was increased in IGF-I Tg mice by ~40%. Oligodendrocyte number in TNF-α/IGF-I Tg mice was almost as twice many as that in TNF-α Tg mice. Furthermore, IGF-I overexpression significantly reduced TNF-α-induced increases in apoptotic cell number, active caspase-3 abundance and degraded MBP. Our results indicate that IGF-I is capable of protecting myelin and oligodendrocytes from TNF-α-induced damage in vivo

Complementation of Lymphotoxin α Knockout Mice with Tumor Necrosis Factor–expressing Transgenes Rectifies Defective Splenic Structure and Function

Lymphotoxin (LT)α knockout mice, as well as double LTα/tumor necrosis factor (TNF) knockout mice, show a severe splenic disorganization with nonsegregating T/B cell zones and complete absence of primary B cell follicles, follicular dendritic cell (FDC) networks, and germinal centers. In contrast, as shown previously and confirmed in this study, LTβ-deficient mice show much more conserved T/B cell areas and a reduced but preserved capacity to form germinal centers and FDC networks. We show here that similar to the splenic phenotype of LTβ-deficient mice, complementation of LTα knockout mice with TNF-expressing transgenes leads to a p55 TNF receptor–dependent restoration of B/T cell zone segregation and a partial preservation of primary B cell follicles, FDC networks, and germinal centers. Notably, upon lipopolysaccharide challenge, LTα knockout mice fail to produce physiological levels of TNF both in peritoneal macrophage supernatants and in their serum, indicating a coinciding deficiency in TNF expression. These findings suggest that defective TNF expression contributes to the complex phenotype of the LTα knockout mice, and uncover a predominant role for TNF and its p55 TNF receptor in supporting, even in the absence of LTα, the development and maintenance of splenic B cell follicles, FDC networks, and germinal centers