Matrix iterations and Cichon's diagram

Using matrix iterations of ccc posets, we prove the consistency with ZFC of some cases where the cardinals on the right hand side of Cichon's diagram take two or three arbitrary values (two regular values, the third one with uncountable cofinality). Also, mixing this with the techniques in J Symb Log 56(3):795-810, 1991, we can prove that it is consistent with ZFC to assign, at the same time, several arbitrary regular values on the left hand side of Cichon's diagram.Comment: 14 pages, 2 figures, article in press for the journal Archive for Mathematical Logi

Template iterations with non-definable ccc forcing notions

We present a version with non-definable forcing notions of Shelah's theory of iterated forcing along a template. Our main result, as an application, is that, if $\kappa$ is a measurable cardinal and $\theta<\kappa<\mu<\lambda$ are uncountable regular cardinals, then there is a ccc poset forcing $\mathfrak{s}=\theta<\mathfrak{b}=\mu<\mathfrak{a}=\lambda$. Another application is to get models with large continuum where the groupwise-density number $\mathfrak{g}$ assumes an arbitrary regular value.Comment: To appear in the Annals of Pure and Applied Logic, 45 pages, 2 figure

Many Different Uniformity Numbers of Yorioka Ideals

Using a countable support product of creature forcing posets, we show that consistently, for uncountably many different functions the associated Yorioka ideals' uniformity numbers can be pairwise different. In addition we show that, in the same forcing extension, for two other types of simple cardinal characteristics parametrised by reals (localisation and anti-localisation cardinals), for uncountably many parameters the corresponding cardinals are pairwise different.Comment: 29 pages, 4 figure

Non-genomic actions of estradiol and 4-OH-tamoxifen on murine breast cancer cells

Estrogens and tamoxifen do not only exert their effects at the genomic level, but also play a role at the cell membrane activating downstream signaling pathways. We recently characterized an estrogen receptor-positive epithelial murine breast cancer cell line, LM05-E. Utilizing this cell line and MCF-7 cells, we compared the non-genomic effects of estradiol and 4-OH-tamoxifen. We showed that, similar to estradiol, tamoxifen activated the MAPK/ERK 1/2 pathway; however, we did not find activation of PI3K/AKT by either estradiol or tamoxifen. Short-term treatments with estradiol stimulated, whereas tamoxifen inhibited cell proliferation. Using pharmacological inhibitors we showed that the effect of estradiol was mediated by the MAPK/ERK 1/2 pathway, but that inhibition of this pathway did not affect tamoxifen. Surprisingly, however, blocking of PI3K/AKT signaling interfered with the inhibitory effect of tamoxifen. Analysis of the involvement of the EGFR support previous findings that designate this receptor as a mediator of the non-genomic effects of estradiol; blocking EGFR also reverses the inhibitory effect of tamoxifen. Finally, matrix metalloproteinases (MMPs) were confirmed to be involved in the proliferative effect of estradiol. These results demonstrated the novel non-genomic effects of tamoxifen and revealed that pathways downstream of EGFR and PI3K/AKT are involved in the inhibition of cell proliferation. Caution should be exercised when analyzing strategies that aim at combining endocrine therapy with specific signaling inhibitors.Fil: Raffo, Diego Alejandro. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Oncología ; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Pontiggia, Osvaldo Alejandro. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Oncología ; ArgentinaFil: Bal, Elisa Dora. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Oncología ; ArgentinaFil: Simian, Marina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Oncología ; Argentin