Pathologies in the sticky limit of hard-sphere-Yukawa models for colloidal fluids. A possible correction

A known `sticky-hard-sphere' model, defined starting from a hard-sphere-Yukawa potential and taking the limit of infinite amplitude and vanishing range with their product remaining constant, is shown to be ill-defined. This is because its Hamiltonian (which we call SHS2) leads to an {\it exact}second virial coefficient which {\it diverges}, unlike that of Baxter's original model (SHS1). This deficiency has never been observed so far, since the linearization implicit in the `mean spherical approximation' (MSA), within which the model is analytically solvable, partly {\it masks} such a pathology. To overcome this drawback and retain some useful features of SHS2, we propose both a new model (SHS3) and a new closure (`modified MSA'), whose combination yields an analytic solution formally identical with the SHS2-MSA one. This mapping allows to recover many results derived from SHS2, after a re-interpretation within a correct framework. Possible developments are finally indicated.Comment: 21 pages, 1 figure, accepted in Molecular Physics (2003

A Peer-reviewed Newspaper About_ Research Values

An interrogation of value and values in contemporary media and digital culture. Publication resulting from research workshop at Brandenburg Center for Media Studies – ZeM, Potsdam, organised in collaboration with Brandenburg Center for Media Studies – ZeM, Potsdam, and transmediale festival for art and digital culture, Berlin

Molecular requirements for the internalisation step of endocytosis: Insights from yeast

10.1016/S0925-4439(01)00028-XBiochimica et Biophysica Acta - Molecular Basis of Disease15353236-257BBAD

The WASp homologue Las17p functions with the WIP homologue End5p/verprolin and is essential for endocytosis in yeast

Current Biology817959-962CUBL

Potential roles for prions and protein-only inheritance in cancer

Inherited mutations are known to cause familial cancers. However, the cause of sporadic cancers, which likely represent the majority of cancers, is yet to be elucidated. Sporadic cancers contain somatic mutations (including oncogenic mutations); however, the origin of these mutations is unclear. An intriguing possibility is that a stable alteration occurs in somatic cells prior to oncogenic mutations and promotes the subsequent accumulation of oncogenic mutations. This review explores the possible role of prions and protein-only inheritance in cancer. Genetic studies using lower eukaryotes, primarily yeast, have identified a large number of proteins as prions that confer dominant phenotypes with cytoplasmic (non-Mendelian) inheritance. Many of these have mammalian functional homologs. The human prion protein (PrP) is known to cause neurodegenerative diseases and has now been found to be upregulated in multiple cancers. PrP expression in cancer cells contributes to cancer progression and resistance to various cancer therapies. Epigenetic changes in the gene expression and hyperactivation of MAP kinase signaling, processes that in lower eukaryotes are affected by prions, play important roles in oncogenesis in humans. Prion phenomena in yeast appear to be influenced by stresses, and there is considerable evidence of the association of some amyloids with biologically positive functions. This suggests that if protein-only somatic inheritance exists in mammalian cells, it might contribute to cancer phenotypes. Here, we highlight evidence in the literature for an involvement of prion or prion-like mechanisms in cancer and how they may in the future be viewed as diagnostic markers and potential therapeutic targets

End13p/Vps4p is required for efficient transport from early to late endosomes in Saccharomyces cerevisiae

Journal of Cell Science114101935-1947JNCS