Data Discovery and Anomaly Detection Using Atypicality: Theory

A central question in the era of 'big data' is what to do with the enormous amount of information. One possibility is to characterize it through statistics, e.g., averages, or classify it using machine learning, in order to understand the general structure of the overall data. The perspective in this paper is the opposite, namely that most of the value in the information in some applications is in the parts that deviate from the average, that are unusual, atypical. We define what we mean by 'atypical' in an axiomatic way as data that can be encoded with fewer bits in itself rather than using the code for the typical data. We show that this definition has good theoretical properties. We then develop an implementation based on universal source coding, and apply this to a number of real world data sets.Comment: 40 page

Neuroprotective Activities of Heparin, Heparinase III, and Hyaluronic Acid on the Aβ42-Treated Forebrain Spheroids Derived from Human Stem Cells

Extracellular matrix (ECM) components of the brain play complex roles in neurodegenerative diseases. The study of microenvironment of brain tissues with Alzheimer’s disease revealed colocalized expression of different ECM molecules such as heparan sulfate proteoglycans (HSPGs), chondroitin sulfate proteoglycans (CSPGs), matrix metalloproteinases (MMPs), and hyaluronic acid. In this study, both cortical and hippocampal populations were generated from human-induced pluripotent stem cell-derived neural spheroids. The cultures were then treated with heparin (competes for Aβ affinity with HSPG), heparinase III (digests HSPGs), chondroitinase (digests CSPGs), hyaluronic acid, and an MMP-2/9 inhibitor (SB-3CT) together with amyloid β (Aβ42) oligomers. The results indicate that inhibition of HSPG binding to Aβ42 using either heparinase III or heparin reduces Aβ42 expression and increases the population of β-tubulin III⁺ neurons, whereas the inhibition of MMP2/9 induces more neurotoxicity. The results should enhance our understanding of the contribution of ECMs to the Aβ-related neural cell death

Additional file 1: of Genetic and cellular studies highlight that A Disintegrin and Metalloproteinase 19 is a protective biomarker in human prostate cancer

Figure S1. Human prostate cancer cells proliferate faster than normal prostate epithelial cells. Cell proliferation was measured by MTS assay 1, 3 and 5 days after cells were seeded (0.25x105 cells/mL on day 0); n = 12 samples/cell type/time point; mean +/- SEM; *p < 0.05. Figure S2. Over-expression of human TNF-α with human ADAM19 in HEK293 cells promotes TNF-α shedding. (A) HEK293 cells were transfected with either empty vector (pCR3.1) or human ADAM19 vector (pCR3.1 hADAM19). Insert shows cytoplasmic staining of over-expressed ADAM19. 100x magnification. (B) Comparison of HEK293 cells transfected with ADAM19 expression vector alone, TNF-α vector alone or co-transfected with both vectors; mean +/- SEM; *p = 0.0004; **p < 0.0001. Figure S3. Transfection efficiency in HEK293 cells 48 h post-transfection. Phase contrast (A) and green fluorescent protein (GFP) positivity (B). 100x magnification. Figure S4. Transfection efficiency in LNCaP cells 48 h post-transfection. Phase contrast (A) and green fluorescent protein (GFP) positivity (B). 100x magnification. (DOCX 1817 kb