Self-Organization Leads to Supraoptimal Performance in Public Transportation Systems

The performance of public transportation systems affects a large part of the population. Current theory assumes that passengers are served optimally when vehicles arrive at stations with regular intervals. In this paper, it is shown that self-organization can improve the performance of public transportation systems beyond the theoretical optimum by responding adaptively to local conditions. This is possible because of a “slower-is-faster” effect, where passengers wait more time at stations but total travel times are reduced. The proposed self-organizing method uses “antipheromones” to regulate headways, which are inspired by the stigmergy (communication via environment) of some ant colonies

Sustained suppression by Foxp3+ regulatory T cells is vital for infectious transplantation tolerance

A new genetic mouse model demonstrates the necessity of Foxp3+ T reg cells for infectious tolerance

STAT1-induced ASPP2 transcription identifies a link between neuroinflammation, cell polarity, and tumor suppression

Inflammation and loss of cell polarity play pivotal roles in neurodegeneration and cancer. A central question in both diseases is how the loss of cell polarity is sensed by cell death machinery. Here, we identify apoptosis-stimulating protein of p53 with signature sequences of ankyrin repeat-, SH3 domain-, and proline-rich region-containing protein 2 (ASPP2), a haploinsufficient tumor suppressor, activator of p53, and regulator of cell polarity, as a transcriptional target of signal transducer and activator of transcription 1 (STAT1). LPS induces ASPP2 expression in murine macrophage and microglial cell lines, a human monocyte cell line, and primary human astrocytes in vitro. LPS and IFNs induce ASPP2 transcription through an NF-κB RELA/p65-independent but STAT1-dependent pathway. In an LPS-induced maternal inflammation mouse model, LPS induces nuclear ASPP2 in vivo at the blood–cerebral spinal fluid barrier (the brain’s barrier to inflammation), and ASPP2 mediates LPS-induced apoptosis. Consistent with the role of ASPP2 as a gatekeeper to inflammation, ASPP2-deficient brains possess enhanced neuroinflammation. Elevated ASPP2 expression is also observed in mouse models and human neuroinflammatory disease tissue, where ASPP2 was detected in GFAP-expressing reactive astrocytes that coexpress STAT1. Because the ability of ASPP2 to maintain cellular polarity is vital to CNS development, our findings suggest that the identified STAT1/ASPP2 pathway may connect tumor suppression and cell polarity to neuroinflammation