This article argues that there is a consistent description of gravitationally collapsed bodies, including neutron stars above the Tolman-Oppenheimer-Volkoff mass and also supermassive galactic centres, according to which collapse stops before the object reaches its gravitational radius, the density reaching a maximum close to the surface and then decreasing towards the centre. Models for such shell-like objects have been constructed using classic formulations found in the 1939 articles of Oppenheimer-Volkoff and Oppenheimer-Snyder. It was possible to modify the conclusions of the first article by changing the authors’ boundary conditions at r = 0. In the second case we find that the authors’ solution of the field equations needs no changes, but that the choice of their article’s title led many of their successors to believe that it supports the black-hole hypothesis. However, it is easily demonstrated that their final density distribution accords with the shell models found in our articles. Because black holes, according to many formulations, "have no hair", their thermodynamics is rather simple. The kind of collapsar which our models describe are more like main-sequence stars; they have spatiotemporal distributions of pressure, density and temperature, that is they have hair. In this article we shall concentrate on the dynamics of the Oppenheimer-Snyder collapsar; both pressure and temperature are everywhere zero, so there can be no thermodynamics. Only in the time independent case of Oppenheimer-Volkoff type models is it currently feasible to consider some thermodynamic implications; here some valuable new insights are obtained through the incorporation of the Oppenheimer-Snyder dynamics.

Loss-of-function mutations of the spermine synthase gene (SMS) result in Snyder-Robinson Syndrome (SRS), a recessive X-linked syndrome characterized by intellectual disability, osteoporosis, hypotonia, speech abnormalities, kyphoscoliosis, and seizures. As SMS catalyzes the biosynthesis of the polyamine spermine from its precursor spermidine, SMS deficiency causes a lack of spermine with an accumulation of spermidine. As polyamines, spermine and spermidine play essential cellular roles that require tight homeostatic control to ensure normal cell growth, differentiation, and survival. Using patient-derived lymphoblast cell lines, we sought to comprehensively investigate the effects of SMS deficiency on polyamine homeostatic mechanisms including polyamine biosynthetic and catabolic enzymes, derivatives of the natural polyamines, and polyamine transport activity. In addition to decreased spermine and increased spermidine in SRS cells, ornithine decarboxylase activity and its product putrescine were significantly decreased. Treatment of SRS cells with exogenous spermine revealed that polyamine transport was active, as the cells accumulated spermine, decreased their spermidine level, and established a spermidine-to-spermine ratio within the range of wild type cells. SRS cells also demonstrated elevated levels of tissue transglutaminase, a change associated with certain neurodegenerative diseases. These studies form a basis for further investigations into the leading biochemical changes and properties of SMS-mutant cells that potentially represent therapeutic targets for the treatment of Snyder-Robinson Syndrome.