Superlinear urban scaling by functional organization: A metabolic interpretation of sectoral water consumption.

Prevailing view asserts that the disproportionately greater productivities of larger cities, or superlinear urban scaling, are the result of human interactions channeled by urban networks. But this view was established by considering the spatial organization of urban infrastructure and social networks-the urban "arteries" effects-but neglecting the functional organization of urban production and consumption entities-the urban "organs" effects. Here, adopting a metabolic view and using water consumption as a proxy for metabolism, we empirically quantify the scaling of entity number, size, and metabolic rate for the functionally specific urban residential, commercial, public or institutional, and industrial sectors.

IRB Problems and Solutions in Health Communication Research.

In this article, we contribute to the current literature on the difficulties that social scientists encounter with IRBs, but with a focus on the distinct challenges that health communication scholars face in dealing with IRBs at their own institutions and elsewhere. Although health communication researchers, like other communication researchers, can expect to face many of the same challenges that their social science colleagues face during the IRB process, the researcher narratives we present in this article suggest that health communication research presents some distinct challenges because the communication interactions that we investigate occur in highly protected, private spaces, including the medical exam room, online patient forums, and electronic health records. To that end, we present a series of examples in which health communication researchers were able to find solutions or workarounds to the challenges they faced in gaining IRB approval for their research.

E1A oncogene expression inhibits PTHrP P3 promoter activity and sensitizes human prostate cancer cells to TNF-induced apoptosis.

In the advanced stages of prostate cancer, tumor cells can evolve to become androgen-independent and resistant to injury-induced apoptosis. Tumor cell expression of parathyroid hormone-related protein (PTHrP) may contribute to the apoptosis phenotype. Expression of the adenovirus E1A oncogene repressed PTHrP promoter and mRNA expression in human PC-3 prostate cancer cells and increased the caspase 3 activation and sensitivity of these cells to apoptosis triggered by tumor necrosis factor alpha.