What Makes Deviant Places?

Urban safety plays an essential role in the quality of citizens' lives and in the sustainable development of cities. In recent years, researchers have attempted to apply machine learning techniques to identify the role of location-specific attributes in the development of urban safety. However, existing studies have mainly relied on limited images (e.g., map images, single- or four-directional images) of areas based on a relatively large geographical unit and have narrowly focused on severe crime rates, which limits their predictive performance and implications for urban safety. In this work, we propose a novel method that predicts "deviance," which includes formal deviant crimes (e.g., murders) and informal deviant behaviors (e.g., loud parties at night). To do this, we first collect a large-scale geo-tagged dataset consisting of incident report data for seven metropolitan cities, along with corresponding sequential images around incident sites obtained from Google Street View. We then design a convolutional neural network that learns spatio-temporal visual attributes of deviant streets. Experimental results show that our framework is able to reliably recognize real-world deviance in various cities. Furthermore, we analyze which visual attribute is important for deviance identification and severity estimation with respect to social science as well as activated feature maps in the neural network. We have released our dataset and source codes on https://github.com/JinhwiPark/DevianceNet/.

Effects of Low-Lipid Diets on Growth, Haematology, Histology and Immune Responses of Parr-Stage Atlantic Salmon (Salmo salar).

Lipids in fish diets provide energy and play important roles in immunity and metabolism. Atlantic salmon, a species that migrates from freshwater to seawater, requires high energy, especially during smoltification. Juvenile teleosts have low lipid requirements, and a high dietary lipid content is known to have negative effects on their growth and digestion. Therefore, this study evaluated the effect of two commercial rainbow trout feeds (low-lipid, 13.41% and 14.6%) on the growth and immune responses of early parr-stage Atlantic salmon compared to commercial salmon feed (high-lipid, 29.52%). Atlantic salmon parr (weight: 14.56 ± 2.1 g; length: 11.23 ± 0.44 cm) were randomly divided into three groups and fed either one of two commercial rainbow trout feeds (RTF1 and RTF2) or the commercial salmon feed (ASF) for 12 weeks. At the end of the feeding trial, growth, haematology, histology and gene expression analyses were performed. There were no significant differences in weight gain rates or feed efficiency between the groups (p > 0.05). Superoxidate dismutase, glutathione peroxidase, lysozyme and immunoglobulin M activities were not different among the experimental groups (p > 0.05). A histological examination of the liver and intestinal tissues showed no pathological symptoms of inflammatory response or lipid accumulation in any of the groups. In an intestinal transcriptome analysis using RNA-seq, the expression levels of several genes linked to lipids, immune-related proteins, cytokines and chemokines did not differ significantly between the groups (p > 0.05). Commercial rainbow trout feed with low lipid content has no clear negative impact on the development of Atlantic salmon during the early parr stage (14.5 to 39.6 g). This study provides basic information for the development of economical feed for early parr-stage Atlantic salmon.

Streptococcus pneumoniae ClpP protease induces apoptosis via caspase-independent pathway in human neuroblastoma cells: cytoplasmic relocalization of p53.

Streptococcus pneumoniae causes the most severe form of the bacterial meningitis which is the major cause of bacterial meningitis. Virulence factors produced by S. pneumoniae have been known to contribute significantly to the disease process. ClpP protease (ClpP) which is essential for virulence and survival under stress conditions in S. pneumoniae was examined for the ability to induce apoptosis and the mechanism of the induction of apoptosis in human neuron-like cells, SK-N-SH neuroblastoma cells. ClpP inhibited cell growth and induced apoptosis in SK-N-SH cells. Treatment with ClpP resulted in hypodiploid DNA contents, increased Bax/Bcl-2 ratio and induction of reactive oxygen species (ROS) production. The release of cytochrome c from mitochondria into the cytosol, which is an initiator of the activation of caspase cascades, was not observed in ClpP-treated cells. In addition, pretreatment with Z-Val-Ala-Asp-fluoromethylketone (Z-VAD-fmk), a broad spectrum caspase inhibitor, could not rescue apoptotic cells from ClpP toxicity. Coincidently, caspase-3 and -8 activation and cleavage of PARP were not detected. Moreover, caspase independent apoptosis-inducing factor (AIF) was released from mitochondria and translocated to the nucleus in response to ClpP. We also found that ClpP treatment resulted in the increase of p53 activity and cytoplasmic p53 levels were increased by ClpP, suggesting that functional activation of p53 is intact despite increased cytoplasmic accumulation. Taken together, these data suggest that ClpP contributes to neuronal damage in meningitis and provide further insight into the mechanisms underlying action of pneumococcal virulence factors during bacterial pathogenesis.