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Cardiovascular diseases and cancer represent respectively the first and second cause of death in industrialized countries. These two conditions may become synergistic when cardiovascular complications of anti-cancer therapy are considered. More than 70 of childhood and 50 of adult cancer patients can be cured, however this important success obtained by the biological and medical research is obfuscated by emerging findings of early and late morbidity due to cardiovascular events. Although anthracyclines are effective drugs against cancer a dose-dependent cardiotoxic effects whose mechanism has not been elucidated resulting in failure of therapeutic interventions limit their use. Unexpectedly, tyrosine/ kinase inhibitors (TKIs) aimed at molecularly interfering with oncogenic pathways, have been implicated in cardiac side effects. Possible explanations of this phenomenon have been ambiguous, further strengthening the need to deepen our understanding on the mechanism of cardiotoxicity. In addition to a detailed description of anthracyclines and TKIs-related cardiovascular effects, the present review highlights recent observations supporting the hypothesis that the cellular target of anthracyclines and TKIs may include myocardial compartments other than parenchymal cells. The demonstration that the adult mammalian heart possesses a cell turnover regulated by primitive cells suggests that this cell population may be implicated in the onset and development of cardiovascular effects of anti-cancer strategies. The possibility of preventing cardiotoxicity by preservation and/or expansion of the resident stem cell pool responsible for cardiac repair may open new therapeutic options to unravel an unsolved clinical issue.

Hydrostatic pressure or anisotropic stress can modify the electronic properties of a metal, thus inducing a change in the topology of its Fermi surface. In the case of low-dimensional anisotropic superconductors (such as high- T c cuprates, some organic salts, or heavy Fermion compounds), such changes result in a nonmonotonic dependence of several properties on the critical parameter z , measuring the distance of the chemical potential from the electronic topological transition (ETT). This has to be contrasted with the monotonic, nearly step-like z -dependence of the same quantities in the 3D case. Such a non-monotonic behavior is in agreement with the trend observed for T c as a function of pressure and other material specific quantities in several high- T c cuprate compounds. On the other hand, higher pressures than those reported in the literature (∼ 10 kbar) should be investigated, in order to find evidence for ETT effects in the BEDT-TTF-based salts.

There are many data on the activity of the RBgene in neural differentiation and apoptosis, but the role of pRb2/p130 in neuronal and glial maturation has been far less investigated. To elucidate the role of pRb2/p130 in astrocyte development we overexpressed this protein in astrocytoma and normal astrocyte cultures by adenoviral-mediated gene transfer. In astrocytoma cells, p130/RB2 overexpression resulted in a significant reduction of cell growth and in an increased G0/G1cell population. We did not observe any induction of programmed cell death as determined by TUNEL reaction. Interestingly, pRb2/p130 overexpression induced astrocyte differentiation. Astrocyte cell cycle arrest and differentiation seemed to proceed through a way distinct from the p53 pathway.

The boson–fermion model is studied within the mean-field approximation including Pauli principle effects in the boson energy renormalization and Coulomb short-range repulsion among fermions and bosons. It is shown that there is a finite critical temperature at which Cooper pairing occurs accompanied by the divergence of the renormalized boson propagator at q=0 and ω=0. The chemical potential, the entropy and the specific heat are also discussed.