population may be identified by the expression of the cell surface marker CD133 and by absence of CD45 and CD31.CD133 expression has been reported in several tumor tissues, including colon and liver cancers.Aim of our study was to investigate if there is a CD133+/ CD45-/CD31-cell population in hepatic metastasis from colon cancer versus normal peritumoral samples harvested from patients subjected to hepatic resection.Methods: Tumor and normal samples were obtained from consenting patients diagnosed with hepatic metastasis from colon cancer.Samples were mechanically fragmented and, then, digested by collagenase I (0,2%) at 37°C, for 90 min.The cell suspensions (from tumor and normal tissue) were filtered through cell strainers and characterized by flow cytometry, using antibodies against CD133, CD45 and CD31.Results: We collected 5 hepatic metastasis from colon cancer samples (2 males/3females).Median age of the patients was 55,7 years.The CD133+/CD45-/ CD31-cell fraction resulted to be 12,2% (ranging from 6% to 16%) in metastasis specimens compared with 0,15% (ranging from 0% to 0,45%) in normal liver tissue.The difference between both groups was significant .Conclusions: Our preliminary data confirm a significant higher proportion of CD133+/CD45-/CD31-cells in metastasis samples respectively to healthy tissues.The high prevalence of CD133+ positive cells within metastasis reinforces the "CSC theory", a subpopulation of tumorigenic cells responsible for tumor aggressiveness.

In this paper, we investigate Galton-Watson branching processes in random environments. In the case where the environmental process is a Markov chain which is positive recurrent or has a transition matrix Q (θ,α) such that sup,, Q (θ,α) > 0 for some a, we prove that the model has the asymptotic behavior being similar to that of Galton-Watson branching processes. In other case where the environments are non-stationary independent, the sufficient conditions are obtained for certain extinction and uncertain extinction for the model.

In this paper, the ruin distributions were analyzed, including the distribution of surplus immediately before ruin, the distribution of claim at the time of ruin, the distribution of deficit, and the distribution of surplus at the beginning of the claim period before ruin. Several integral equations for the ruin distributions were derived and some solutions under special conditions were obtained.

Exposure of cells to arsenicals activates multiple stress pathways resulting in the induction of specific genes whose identity and role in the adaptation to arsenical-induced cellular stress are poorly understood. We report here the identification of a novel gene encoding an arsenite-inducible, cysteine- and histidine-rich RNA-associated protein, AIRAP, that is conserved among mammals, Drosophila and C elegans. Immunochemistry and cell fractionation experiments indicate that, when induced, AIRAP is present in both the nucleus and the cytoplasm, and cross-linking experiments indicate that it associates with RNA in vivo. The expression of a C elegans homologue of AIRAP, aip-1, is also induced by exposure to arsenite, and expression of an aip-1::gfp transgene is most pronounced in hypodermal cells. RNA-mediated interference (RNAi) of aip-1 lowers the resistance of nematodes to arsenite yet does not appear to affect viability under standard growth conditions. These experiments suggest a role for AIRAP/AIP-1 in protecting cells from the toxic effects of arsenite.