Estudio cualitativo sobre la oferta y la demanda de servicios educativos en el mercado electrónico mendocino

Durante la última década, el creciente auge de las redes de información ha llevado consigo un marcado acento en la utilización de este medio como reductor de costes y maximizador de beneficios para el desarrollo de un mercado educativo.Una variada composición y estrategia de nuevas ofertas al respecto se soportan, actualmente, en las tecnologías de comunicación e información, creando una demanda asociada a éstas. Observar, clasificar, encontrar invariantes, es parte de un análisis cualitativo de estudio para este nuevo mercado y su auge en Mendoza. Este es un trabajo que complementa al ya presentado oportunamente sobre “perfil del consumidor mendocino en Internet". Algunas de las preguntas que se formulan indefectiblemente al respecto son: ¿cómo es el comportamiento de la demanda educativa en este nuevo mercado electrónico de educación?; ¿cómo responde la oferta a éste tipo de demanda?; ¿cuál es su composición, niveles del sistema educativo y tipos: formal e informal, público y privado, etc.?; ¿qué parámetros de calidad conlleva la oferta de bienes y servicios educativos?; ¿cuál es el grado de penetración de dicha oferta?; ¿cuál es el grado de permanencia, por parte del consumidor del servicio?; ¿quiénes y cuál es el perfil de los demandantes de servicios en e-educación?; ¿cuál es el grado de satisfacción por parte de quienes adquieren servicios y/o productos educativos? y otras más. Se pretende que dichos resultados se transfieran al medio generando mayores oportunidades laborales, al interpretar a esto como un mercado asociado a un nuevo tipo de oferta de servicios profesionales, de forma que las PyME que quieran explotar esta temática, reduzcan la incertidumbre propia de un mercado poco o escasamente estudiado.During the last decade, in the supreme growing of information nets has taking with it defining accent in the using of this medium as a cost reducer and getting the maxims benefit for the development of educative market.A variety composition and strategy of the new offer respecting each others, actually, in the technologies of communication and information, crating a demand associated to these ones. Observe, calificate, find invariants, it’s a part of a qualitative analysis of the study for this mew market and it’s supreme in Mendoza. This is a job that completes the already presented about “the profile of the mendocinian on internet". Some of the questions that are formuled unfailingly to respect are: How is the behavior of educative demand in this new electronic market? How does the offer to this kind of demand respond? Which is the penetration grade of this offer? Which is the permanence grade from part of the services consumers in education? Which is the satisfaction grade from part of who get the services and/or educative products? It pretends that this results be transferred to the medium making majors workable opportunities in order to interpret this as a market associating a new kind of professional services offers, the from that the PyME that want to exploits this topic, reduce the own uncertainty of a few sanctity study market

The recruitment and activation of phosphatidylinositol 4-phosphate 5-kinases α critically regulate CD28-dependent signaling responses

CD28 costimulatory receptor is a crucial determinant of the outcome of T lymphocyte activation. The engagement of CD28 by its natural ligands, B7.1/CD80 or B7.2/CD86, expressed on the surface of professional APC, lowers T cell receptor (TCR) activation threshold, thus leading to the enhancement of early signalling events necessary for efficient cytokine production, cell cycle progression, survival and regulation of T cells effector responses. CD28 is also able to act as a unique signalling receptor and to deliver TCR-independent autonomous signals, which account for its critical role in the regulation of pro-inflammatory cytokine/chemokine production and T cell survival. Most of the CD28-dependent signalling functions are initiated by the recruitment and activation of class IA phosphatidylinositol 3-kinase (PI3K), The intracytoplasmic domain of CD28 contains a N-terminal YMNM motif that following phosphorylation binds the p85 subunit of phosphatidylinositol 3-kinase (PI3K). Once activated, PI3K catalyzes the conversion of phosphatidylinositol 4,5-biphosphate (PIP2) to phosphatidylinositol 3,4,5-triphosphate (PIP3) and generates the docking sites for key signalling proteins. PIP2 plays a critical role in the regulation of both cytoskeleton dynamics and second messenger generation. Indeed, PIP2 is the common source for two major distinct signalling cascades involving PI3K and PLCγ1 that often colocalize in the same signalling complexes competing for the common pool of substrate. Consequently, PIP2 levels decrease following receptor activation, thus suggesting that stimulation of PIP2 synthesis may be an essential regulatory step to sustain the activation of both PI3K and PLCγ1 following CD28 engagement. The main biosynthetic pathway of PIP2 involves phosphorylation of phosphatidylinositol 4-monophosphate (PI4P) at the D5 position of the inositol ring by PIP5K. Three PIP5K isoforms (α, β and γ) have been identified. Several data obtained in different cell systems evidenced differential subcellular localizations of each isoform. PIP5Kα, for instance, is localized at the plasma membrane, where it guarantees the local availability of PIP2. Here we show that CD28 stimulation by both B7.1/CD80 or agonistic Abs induces the recruitment and activation of PIP5Kα in human primary CD4+ T lymphocytes. This event leads to the neo-synthesis of PIP2 that is consumed by CD28-activated PI3K. By either small interference RNA (siRNA)-driven cell silencing or overexpressing a kinase dead mutant, we evidenced that PIP5Kα activation is required for both CD28 autonomous signals regulating IL-8 gene expression as well as for CD28/TCR-induced Ca2+ mobilization, NF-AT nuclear translocation and IL-2 gene transcription. Our findings identify PIP5Kα as a critical mediator of CD28-dependent responses

CD4-Lck Through TCR and in the Absence of Vav Exchange Factor Induces Bax Increase and Mitochondrial Damage

AbstractIn the present study, we aimed to demonstrate that CD4 may represent a critical turning point that governs the apoptotic and survival programs in T cells, without modifying the physical association with the TCR-CD3 complex. To address this issue, we have explored the possibility that the activation of CD4 may transduce apoptotic signals unless signaling effectors neutralize them. Our data show that in Jurkat T cells CD4 engagement by Leu3a mAb results in a rapid and strong increase of Lck kinase activity, subsequent alterations of mitochondrial membrane potential, and apoptosis. Critical parameters are coassociation of CD4/Lck with TCR/CD3 and up-regulation of the proapoptotic protein Bax. Indeed, Leu3a-mediated Lck activation failed to induce apoptotic features in Jurkat cells either defective for TCR/CD3 or overexpressing the antiapoptotic protein Bcl-2. Furthermore, we demonstrate that Leu3a treatment of Jurkat cells overexpressing Vav results in the inhibition of mitochondrial damage and apoptosis; this rescue effect is accompanied with a significant decrease of Bax expression observed in apoptotic cells. Our evidence that the activation of Lck activates in T cells apoptotic pathways which are counteracted by Vav, a signaling molecule that cooperates with CD28 to boost TCR signals, suggests a novel role for costimulation in protecting T cells from CD4-mediated cell death

FT-IR characterization of antimicrobial hybrid materials through sol-gel synthesis

Silica/polycaprolactone and titania/polycaprolactone hybrid organic/inorganic amorphous composites were prepared via a sol-gel method starting from a multi-element solution containing tetramethyl orthosilicate (TMOS) or titanium butoxide (TBT), polycaprolactone (PCL), water and methylethylketone (MEK). The molecular structure of the crosslinked network was based on the presence of the hydrogen bonds between organic/inorganic elements as confirmed by Fourier Transform Infra-Red (FT-IR) analysis. In particular, the structure of crosslinked network was realized by hydrogen bonds between the X-OH (X = Si or Ti) group (H donator) in the sol-gel intermediate species and ester groups (H-acceptors) in the repeating units of the polymer. The morphology of the hybrid materials; pore size distribution, elemental homogeneity and surface features, was studied by scanning electron microscopy/energy dispersive spectroscopy (SEM/EDS) and by atomic force microscopy (AFM). The bioactivity of the synthesized hybrid materials was confirmed by observing the formation of a layer of hydroxyapatite (HAP) on the surface of the samples soaked in a simulated body fluid. The antimicrobial behavior of synthetized hybrids was also assessed against Escherichia coli bacteria. In conclusion, the prepared hybrid materials are proposed for use as future bone implants

Caratterizzazione del sistema attivatore del plasminogeno nella progressione metastatica del cancro prostatico umano

GnRH analogues are used for the treatment of prostate cancer (PCa) because their ability to suppress the activity of the pituitary-testicular axis, with consequent blockade of testosterone production. However, after an initial responsiveness to hormonal deprivation, PCa progresses and then metastatises. It is known that the system of the plasminogen activator (uPA, uPA inhibitors PAI-1/2 and uPA receptor, uPAR) has been involved in the local degradation of the extracellular matrix and PCa progression and metastases. Studies performed in our laboratory have demonstrated the presence of GnRH receptors, suggesting a direct effect of GnRH analogues in inhibiting the proliferation of human PCa cell lines. The aim of this study was to test the effect of an agonist (Leuprolide) and an antagonist (Cetrorelix) of GnRH on uPA/uPAR and PAI-1 expression and activity, on the migratory and invasion capabilities in the two androgen-independent cell lines, DU145 and PC3 cells. The results obtained in DU145 and PC3 cells show that both Leuprolide and Cetrorelix: 1) significantly decrease the enzymatic activity of uPA; 2) induce a marked decrease of uPA and a significant increase of PAI-1 protein levels; 3) increase the presence of soluble uPAR in the cell media; 4) decrease the migratory and invasion capabilities. In conclusions, GnRH analogues might interfere with the mechanisms of metastatic progression of human androgen-independent PCa by inhibiting the activity of the plasminogen activator system

Could polyphenols really be a good radioprotective strategy?

Currently, radiotherapy is one of the most effective strategies to treat cancer. However, deleterious toxicity against normal cells indicate for the need to selectively protect them. Reactive oxygen and nitrogen species reinforce ionizing radiation cytotoxicity, and compounds able to scavenge these species or enhance antioxidant enzymes (e.g., superoxide dismutase, catalase, and glutathione peroxidase) should be properly investigated. Antioxidant plant-derived compounds, such as phenols and polyphenols, could represent a valuable alternative to synthetic compounds to be used as radio-protective agents. In fact, their dose-dependent antioxidant/pro-oxidant efficacy could provide a high degree of protection to normal tissues, with little or no protection to tumor cells. The present review provides an update of the current scientific knowledge of polyphenols in pure forms or in plant extracts with good evidence concerning their possible radiomodulating action. Indeed, with few exceptions, to date, the fragmentary data available mostly derive from in vitro studies, which do not find comfort in preclinical and/or clinical studies. On the contrary, when preclinical studies are reported, especially regarding the bioactivity of a plant extract, its chemical composition is not taken into account, avoiding any standardization and compromising data reproducibility

Both Maturation and Survival of Human Dendritic Cells are Impaired in the Presence of Anergic/Suppressor T Cells

T cell suppression is a well established phenomenon, but the mechanisms involved are still a matter of debate. Mouse anergic T cells were shown to suppress responder T cell activation by inhibiting the antigen presenting function of DC. In the present work we studied the effects of co-culturing human anergic CD4+ T cells with autologous dendritic cells (DC) at different stages of maturation. Either DC maturation or survival, depending on whether immature or mature DC where used as APC, was impaired in the presence of anergic cells. Indeed, MHC and costimulatory molecule up-regulation was inhibited in immature DC, whereas apoptotic phenomena were favored in mature DC and consequently in responder T cells. Defective ligation of CD40 by CD40L (CD154) was responsible for CD95-mediated and spontaneous apoptosis of DC as well as for a failure of their maturation process. These findings indicate that lack of activation of CD40 on DC by CD40L-defective anergic cells might be the primary event involved in T cell suppression and support the role of CD40 signaling in regulating both activation and survival of DC

Physicochemical Properties of PEG-Based Inorganic Hybrids Obtained via Sol-Gel

Organic-inorganic composites can be conveniently obtained by sol-gel recipes. They can find interesting applications in several fields, including drug delivery, scaffolding, bio-sensing, energetics, etc. Herein, we reconsider and reinvestigate our previous work in the field, by considering the sol-gel synthesis and physicochemical characterization of class-I organic-inorganic hybrids, and by trying to highlight some unifying elements that can be of help for the development of more efficient and precise synthesis methods. Systems based on poly(ethylene glycol) with SiO2 and ZrO2 as the ceramic phase will be discussed. Emphasis will be put on the role played by solid-state NMR spectroscopy in unveiling the interactions at the base of hybrid formation

The activation of Csk by CD4 interferes with TCR-mediated activatory signaling

CD4-Lck recruitment to TCR/CD3, as well as Lck activation is essential for T cell activation. Indeed, the blockage of CD4-Lck recruitment to TCR during antigen recognition exerts a drastic inhibitory effect on T cell activation by interfering with both early and late phases of T cell signaling. In the present work, we report a novel inhibitory mechanism by which CD4 can shut down proximal T cell-activating signals. Indeed, we show that upon ligation of CD4 by antibodies the inhibitory kinase, p50csk, is strongly induced and prolonged during the time. In contrast, p50csk was not activated when TCR and CD4 were properly engaged by their ligands. We also demonstrate that anti-CD4 treatment stimulated Csk kinase associated to the membrane adapter, PAG/Cbp, without affecting the total amount of Csk bound to PAG/Cbp. As a consequence, early tyrosine phosphorylation events as well as downstream signaling pathways leading to IL-2 gene expression induced by TCR were inhibited in anti-CD4 pretreated cells. We suggest a new model to explain the activation of negative signals by CD4 molecule