Since DeepMind’s AlphaZero, Zero learning quickly became the state-of-the-art method for many board games. It can be improved using a fully convolutional structure (no fully connected layer). Using such an architecture plus global pooling, we can create bots independent of the board size. The training can be made more robust by keeping track of the best checkpoints during the training and by training against them. Using these features, we release Polygames, our framework for Zero learning, with its library of games and its checkpoints. We won against strong humans at the game of Hex in 19 × 19, including the human player with the best ELO rank on LittleGolem; we incidentally also won against another Zero implementation, which was weaker than humans: in a discussion on LittleGolem, Hex19 was said to be intractable for zero learning. We also won in Havannah with size 8: win against the strongest player, namely Eobllor, with excellent opening moves. We also won several first places at the TAAI 2019 competitions and had positive results against strong bots in various games.

Maintenance of epithelial polarity depends on the correct localization and levels of polarity determinants. The evolutionarily conserved transmembrane protein Crumbs is crucial for the size and identity of the apical membrane, yet little is known about the molecular mechanisms controlling the amount of Crumbs at the surface. Here, we show that Crumbs levels on the apical membrane depend on a well-balanced state of endocytosis and stabilization. The adaptor protein 2 (AP-2) complex binds to a motif in the cytoplasmic tail of Crumbs that overlaps with the binding site of Stardust, a protein known to stabilize Crumbs on the surface. Preventing endocytosis by mutation of AP-2 causes expansion of the Crumbspositive plasma membrane domain and polarity defects, which can be partially rescued by removing one copy of crumbs. Strikingly, knocking down both AP-2 and Stardust leads to the retention of Crumbs on the membrane. This study provides evidence for a molecular mechanism, based on stabilization and endocytosis, to adjust surface levels of Crumbs, which are essential for maintaining epithelial polarity.

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Summary. Early postnatal use of dexamethasone has recently been shown to be effective in improving the pulmonary status in premature infants with respiratory distress syndrome (RDS). To study the effect of dexamethasone on pulmonary inflammatory responses, we studied ten infants treated with dexamethasone and ten infants without this treatment. Serial tracheal aspirates were obtained for cell counts, neutrophil counts, total protein concentrations, and leukotriene B 4 (LTB 4 ) and 6-keto prostaglandin (PG)F 1␣ levels before and after starting the study. Infants in the dexamethasone-treated group required significantly lower mean airway pressures for ventilation and had lower P a CO 2 values from day 3 to day 14 than infants in the control group, suggesting better pulmonary function. For infants in the dexamethasone group, the tracheal aspirates showed significantly lower cell and neutrophil counts, protein concentrations, and 6-keto-PGF 1␣ and LTB 4 levels than in the control group. We conclude that early postnatal dexamethasone therapy may lessen lung inflammation and improve pulmonary function in infants with RDS.

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