Synchronization of passes in event and spatiotemporal soccer data

The majority of soccer analysis studies investigates specific scenarios through the implementation of computational techniques, which involve the examination of either spatiotemporal position data (movement of players and the ball on the pitch) or event data (relating to significant situations during a match). Yet, only a few applications perform a joint analysis of both data sources despite the various involved advantages emerging from such an approach. One possible reason for this is a non-systematic error in the event data, causing a temporal misalignment of the two data sources. To address this problem, we propose a solution that combines the SwiftEvent online algorithm (Gensler and Sick in Pattern Anal Appl 21:543–562, 2018) with a subsequent refinement step that corrects pass timestamps by exploiting the statistical properties of passes in the position data. We evaluate our proposed algorithm on ground-truth pass labels of four top-flight soccer matches from the 2014/15 season. Results show that the percentage of passes within half a second to ground truth increases from 14 to 70%, while our algorithm also detects localization errors (noise) in the position data. A comparison with other models shows that our algorithm is superior to baseline models and comparable to a deep learning pass detection method (while requiring significantly less data). Hence, our proposed lightweight framework offers a viable solution that enables groups facing limited access to (recent) data sources to effectively synchronize passes in the event and position data

β-Catenin Signaling Increases during Melanoma Progression and Promotes Tumor Cell Survival and Chemoresistance

Beta-catenin plays an important role in embryogenesis and carcinogenesis by controlling either cadherin-mediated cell adhesion or transcriptional activation of target gene expression. In many types of cancers nuclear translocation of beta-catenin has been observed. Our data indicate that during melanoma progression an increased dependency on the transcriptional function of beta-catenin takes place. Blockade of beta-catenin in metastatic melanoma cell lines efficiently induces apoptosis, inhibits proliferation, migration and invasion in monolayer and 3-dimensional skin reconstructs and decreases chemoresistance. In addition, subcutaneous melanoma growth in SCID mice was almost completely inhibited by an inducible beta-catenin knockdown. In contrast, the survival of benign melanocytes and primary melanoma cell lines was less affected by beta-catenin depletion. However, enhanced expression of beta-catenin in primary melanoma cell lines increased invasive capacity in vitro and tumor growth in the SCID mouse model. These data suggest that beta-catenin is an essential survival factor for metastatic melanoma cells, whereas it is dispensable for the survival of benign melanocytes and primary, non-invasive melanoma cells. Furthermore, beta-catenin increases tumorigenicity of primary melanoma cell lines. The differential requirements for beta-catenin signaling in aggressive melanoma versus benign melanocytic cells make beta-catenin a possible new target in melanoma therapy