JSTOR is a not-for-profit service that helps scholars, researchers, and students discover, use, and build upon a wide range of content in a trusted digital archive. We use information technology and tools to increase productivity and facilitate new forms of scholarship. For more information about JSTOR, please contact support@jstor.org.. American Risk and Insurance Association is collaborating with JSTOR to digitize, preserve and extend access ABSTRACT The service sector of the world economy has grown substantially since World War II. The worldwide insurance industry has had an average annual growth rate of over 10 percent since 1950. During the mid-1980s, the international life insurance industry grew at an average annual rate greater than 25 percent. This article identifies factors that lead to variations in the demand for life insurance across countries. Important factors are found to be the dependency ratio, national income, government spending on social security, inflation, the price of insurance, and whether Islam is the predominant religion in a country.

We report the presence of defects in CH3NH3PbI3, which is one of the main factors that deteriorates the performance of perovskite solar cells.

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Mig6 is a feedback inhibitor that directly binds, inhibits and drives internalization of ErbB-family receptors. Mig6 selectivity targets activated receptors. Here we find that the EGF receptor phosphorylates Mig6 on Tyr394, and that this phosphorylation is primed by prior phosphorylation of an adjacent residue, Tyr395, by Src. Crystal structures of human EGFR–Mig6 complexes reveal the structural basis for enhanced phosphorylation of primed Mig6 and show how Mig6 rearranges after phosphorylation by EGFR to effectively irreversibly inhibit the same receptor that catalyzed its phosphorylation. This dual phosphorylation site allows Mig6 to inactivate EGFR in a manner that requires activation of the target receptor and can be modulated by Src. Loss of Mig6 is a driving event in human cancer; analysis of 1057 gliomas reveals frequent focal deletions of ERRFI, the gene that encodes Mig6, in EGFR-amplified glioblastomas.