The HIV BioBank represents a novel approach to HIV research that might be of general interest not only for basic and clinical research teams working on HIV, but also for those groups trying to establish large networks focused on research on specific clinical problems. It also represents a model to stimulate cooperative research among large numbers of research groups working as a network on specific clinical problems. The main objective of this article is to show the structure and function of the HIV BioBank that allow it to very efficiently release samples to different research project not only in Spain but also in other countries.

A new family of amine- and ammonium-terminated carbosilane dendrimers of the type Gn-[Si(CH2)3N(Et)CH2CH2NMe2]x and Gn-{[Si(CH2)(3)N+R(Et)CH2CH2N+RMe2]x(X-)y} (where n = 1, 2 and 3; R = H, X = Cl; R = Me, X = I) respectively has been synthesized by hydrosilylation of N,N-dimethyl-N'-allyl-N'-ethyl-ethylenediamine, [(CH2=CH-CH2)(Et)N(CH2)2NMe2] with the corresponding hydride-terminated dendrimers and subsequent quaternization with HCl or MeI. Quaternized dendrimers are soluble and stable in water or other protic solvents for long time periods. The antibacterial properties of the quaternary ammonium functionalized dendrimers have been evaluated showing that they act as potent biocides in which the multivalency along with the biopermeability of the carbosilane dendritic skeleton play an important role in the antibactericidal activity of these compounds.

We have analyzed the intracellular signals that allow lymphoblasts from Alzheimer's disease (AD) patients to escape from serum deprivation-induced apoptosis. The following observations suggested that modulation of ERK1/2 activity by Ca(2+)/calmodulin (CaM) is involved in preventing apoptosis: (i) ERK1/2 activity seems to support lethality in control cells, as PD98059, the inhibitor of the activating MEK prevented cell death; (ii) control cells show a persistent and higher stimulation of ERK1/2 than that of AD cells in the absence of serum; (iii) CaM antagonists have no effects on control cells, but sensitize AD cells to death induced by serum withdrawal and increased ERK1/2 phosphorylation, and (iv) no apoptotic effects of CaM antagonists were observed in AD cells treated with PD98059. These results suggest the existence of an activation threshold of the ERK1/2 pathway setting by Ca(2+)/CaM-dependent mechanisms, which appears to be the critical factor controlling cell survival or death decision under trophic factor withdrawal.