Chromosome Instability and Mosaic Aneuploidy in Neurodegenerative and Neurodevelopmental Disorders.

Evidence from multiple laboratories has accumulated to show that mosaic neuronal aneuploidy and consequent apoptosis characterizes and may underlie neuronal loss in many neurodegenerative diseases, particularly Alzheimer's disease and frontotemporal dementia. Furthermore, several neurodevelopmental disorders, including Seckel syndrome, ataxia telangiectasia, Nijmegen breakage syndrome, Niemann-Pick type C, and Down syndrome, have been shown to also exhibit mosaic aneuploidy in neurons in the brain and in other cells throughout the body. Together, these results indicate that both neurodegenerative and neurodevelopmental disorders with apparently different pathogenic causes share a cell cycle defect that leads to mosaic aneuploidy in many cell types.

Organic materials database: An open-access online database for data mining.

We present an organic materials database (OMDB) hosting thousands of Kohn-Sham electronic band structures, which is freely accessible online at http://omdb.diracmaterials.org.

A Bayesian Additive Model for Understanding Public Transport Usage in Special Events.

Public special events, like sports games, concerts and festivals are well known to create disruptions in transportation systems, often catching the operators by surprise. Although these are usually planned well in advance, their impact is difficult to predict, even when organisers and transportation operators coordinate. The problem highly increases when several events happen concurrently.

The N Terminus of the Retinoblastoma Protein Inhibits DNA Replication via a Bipartite Mechanism Disrupted in Partially Penetrant Retinoblastomas.

The N-terminal domain of the retinoblastoma (Rb) tumor suppressor protein (RbN) harbors in-frame exon deletions in partially penetrant hereditary retinoblastomas and is known to impair cell growth and tumorigenesis. However, how such RbN deletions contribute to Rb tumor- and growth-suppressive functions is unknown. Here we establish that RbN directly inhibits DNA replication initiation and elongation using a bipartite mechanism involving N-terminal exons lost in cancer.