No absorption in de Sitter space

We study the wave equation for a minimally coupled massive scalar in D-dimensional de Sitter space. We compute the absorption cross section to investigate its cosmological horizon in the southern diamond. By analogy of the quantum mechanics, it is found that there is no absorption in de Sitter space. This means that de Sitter space is usually in thermal equilibrium, like the black hole in anti de Sitter space. It confirms that the cosmological horizon not only emits radiation but also absorbs that previously emitted by itself at the same rate, keeping the curvature radius of de Sitter space fixed.Comment: 11 pages, REVTE

Safe access to basic infrastructure: more than pipes and taps [Chapter 8]

Building on a growing movement within developing countries in Latin America, Africa, and Asia-Pacific, as well as Europe and North America, this book documents cutting edge practice and builds theory around a rights based approach to women’s safety in the context of poverty reduction and social inclusion. Drawing upon two decades of research and grassroots action on safer cities for women and everyone, this book is about the right to an inclusive city. The first part of the book describes the challenges that women face regarding access to essential services, housing security, liveability and mobility. The second part of the book critically examines programs, projects and ideas that are working to make cities safer. Building Inclusive Cities takes a cross-cultural learning perspective from action research occurring throughout the world and translates this research into theoretical conceptualizations to inform the literature on planning and urban management in both developing and developed countries. This book is intended to inspire both thought and action

Partial Loss of USP9X Function Leads to a Male Neurodevelopmental and Behavioral Disorder Converging on Transforming Growth Factor β Signaling

The X-chromosome gene USP9X encodes a deubiquitylating enzyme that has been associated with neurodevelopmental disorders primarily in female subjects. USP9X escapes X inactivation, and in female subjects de novo heterozygous copy number loss or truncating mutations cause haploinsufficiency culminating in a recognizable syndrome with intellectual disability and signature brain and congenital abnormalities. In contrast, the involvement of USP9X in male neurodevelopmental disorders remains tentative. We used clinically recommended guidelines to collect and interrogate the pathogenicity of 44 USP9X variants associated with neurodevelopmental disorders in males. Functional studies in patient-derived cell lines and mice were used to determine mechanisms of pathology. Twelve missense variants showed strong evidence of pathogenicity. We define a characteristic phenotype of the central nervous system (white matter disturbances, thin corpus callosum, and widened ventricles); global delay with significant alteration of speech, language, and behavior; hypotonia; joint hypermobility; visual system defects; and other common congenital and dysmorphic features. Comparison of in silico and phenotypical features align additional variants of unknown significance with likely pathogenicity. In support of partial loss-of-function mechanisms, using patient-derived cell lines, we show loss of only specific USP9X substrates that regulate neurodevelopmental signaling pathways and a united defect in transforming growth factor β signaling. In addition, we find correlates of the male phenotype in Usp9x brain-specific knockout mice, and further resolve loss of hippocampal-dependent learning and memory. Our data demonstrate the involvement of USP9X variants in a distinctive neurodevelopmental and behavioral syndrome in male subjects and identify plausible mechanisms of pathogenesis centered on disrupted transforming growth factor β signaling and hippocampal function