1,029 research outputs found

    Dynamic response studies on aggregation and breakage dynamics of colloidal dispersions in stirred tanks

    No full text
    Aggregation and breakage of aggregates of fully destabilized polystyrene latex particles in turbulent flow was studied experimentally in both batch and continuous stirred tanks using small-angle static light scattering. It was found that the steady-state values of the root-mean-square radius of gyration are fully reversible upon changes of stirring speed as well as solid volume fraction. Steady-state values of the root-mean-square radius of gyration were decreasing with decreasing solid volume fraction as well as with increasing stirring speed. Moreover, it was found that the steady-state structure and shape of the aggregates is not influenced by the applied stirring speed

    Effect of selective tachykinin receptor antagonists on the growth of human skin fibroblasts.

    No full text
    The effect of synthetic selective tachykinin receptor antagonists was studied on the growth of cultured human skin fibroblasts (HF). Selective antagonists for the NK1 receptor ([D-Pro4, D-Trp7,9,Phe11]-SP(4-11), GR71251 and L 668,169) and the NK2 receptor (L 659,877) were tested against Substance P (SP), against the selective NK1 receptor agonist [beta-Ala4,Sar9, Met(O2)11]-SP(4-11) and against basic Fibroblast Growth Factor (bFGF). All the selective NK1 receptor antagonists, tested at the concentration of 10(-5)M, induced a significant displacement to the right of the dose-response curves induced by SP and by the selective NK1 receptor agonist. The selective NK2 receptor antagonist did not modify the proliferative response to the tachykinins used. The growth promoting effect of bFGF was not modified by any of the tachykinin antagonists tested. These results indicate that the newly developed receptor-selective tachykinin antagonists appear to be a useful tool to assess the biological effects of tachykinin in vitro on cultured isolated cells

    Impaired Cerebral Perfusion in Multiple Sclerosis: Relevance of Endothelial Factors

    No full text
    Magnetic resonance imaging techniques measuring in vivo brain perfusion and integrity of the blood-brain barrier have developed rapidly in the past decade, resulting in a wide range of available methods. This review first discusses their principles, possible pitfalls, and potential for quantification and outlines clinical application in neurological disorders. Then, we focus on the endothelial cells of the blood-brain barrier, pointing out their contribution in regulating vascular tone by production of vasoactive substances. Finally, the role of these substances in brain hypoperfusion in multiple sclerosis is discussed

    Nitric oxide in tumor angiogenesis

    No full text
    Nitric oxide (NO), produced from L-arginine by NO synthases (NOS), is a short-lived molecule required for many physiological functions and contributing to different pathological conditions. In the last decade, we and others contributed to demonstrate that NO stimulates angiogenesis and mediates the effect of different angiogenic molecules. In human tumors, NOS expression and activity correlate with tumor growth and aggressiveness through angiogenesis stimulation and regulation of angiogenic factor expression. Interrelations among the NOS pathway, prostanoids and tyrosine kinase receptors have been reported in regulating tumor progression and malignancy. Drugs affecting the NOS pathway may be forseen as anti-tumor strategies able to reduce edema, inhibit angiogenesis and facilitate the delivery of chemotherapeutical agents. Recent developments include research on NOS gene polymorphisms which might become useful biomarkers for predicting cancer susceptibility as well as the role of NO in chemopreventive strategies. © 2008 Springer US

    L'acquisizione sanante tra consulta, strasburgo, palazzo spada, palazzaccio. (fine) o quasi degli incidenti di percorso

    No full text
    Sommario: 1. L'"invenzione" della occupazione appropriativa. - 2. Le ragioni del contrasto tra CEDU e occupazione appropriativa. - 3. L'art. 43 T.U. espropriazione e relativa dichiarazione di incostituzionalità per eccesso di delega. - 4. L'art. 42-bis T.U. espropriazione. 5. Le eccezioni di incostituzionalità sollevate nei confronti dell'art. 42-bis. - 6. La sentenza 71/2015: le ragioni di compatibilità dell'art. 42-bis con gli artt. 3, 42, 97 Cost. - 7. La tematica dell'indennizzo. Dubbi di costituzionalità sui criteri di calcolo del risarcimento da occupazione. - 8. Sulla conformità dell'art. 42-bis con i principi della CEDU. - 9. Su talune incertezze che ancora permangono. - 10. Conclusion

    Nitric oxide modulates the angiogenic phenotype of middle-T transformed endothelial cells.

    No full text
    The role of nitric oxide (NO) in the induction of angiogenesis was evaluated in a murine heart endothelioma cell line (H.end.FB) carrying the mT oncogene. Two clonal derivatives of H.end.FB, H80 and H73, exhibiting different NO synthase (NOS) activities were selected and used in the study. The relationship among NOS activity and tumor cell behaviour (growth, and angiogenic capacity) and the molecular control of gene expression were investigated. H.end.FB and H80 on one side and H73 on the other side exhibited the highest and lowest NOS activity, respectively. Cell growth was inversely correlated to the amount of NO produced by the cell lines. Conversely, in the avascular rabbit cornea assay, H.end.FB and H80 cells were strongly angiogenic, while H73 were poorly angiogenic, indicating that the ability of the cells to induce neovascularization was associated with the extent of NO produced. Consistently, systemic administration to rabbits of the NOS inhibitor N(w)-nitro-L-arginine methyl ester (L-NAME) significantly reduced the angiogenicity of H.end.FB cells. RT-PCR evidenced that H.end.FB expressed mRNA for TGF-beta1 and all VEGF isoforms, VEGF165 being predominantly expressed. NOS inhibition reduced the basal expression of VEGF isoforms, while it markedly potentiated TGF-beta1 expression. These results indicate that the endogenous production of NO in tumor cells can serve as an autocrine/paracrine signalling mechanism of progression, by controlling angiogenic factor/modulator expressio

    Preclinical models to assess the pharmacological properties of NO derivatives

    No full text
    The field of pharmacology of nitric oxide (NO) has various clinical perspectives as cardiovascular and metabolic disorders, neurovascular and neurodegenerative diseases, muscular–skeletal disorders, ocular, respiratory, and a large series of inflammation-related pathologies, and, on top of these, infective and neoplastic diseases. Depending on the pathology and pathophysiological mechanisms, different pharmacological approaches can be developed and used, either to stimulate NO synthases (NOS), improve NO availability and activate downstream NO-related pathways or, on the opposite, to downregulate NOS, scavenge NO, and inhibit NO-related signaling. In either conditions, preclinical tools and models are needed to allow molecule or therapeutic strategy screening, evaluating the relative potency, efficacy, and safety in a reliable, simple, relatively cheap, and not time-consuming manner. Different models have been developed during time, starting from the classic isolated organs maintained in balanced buffers and measuring their typical functional responses as relaxation/contraction. The introduction of cell cultures, genetic manipulation, and molecular studies has allowed to go in deep detail on the cellular and molecular mechanisms controlling upstream and downstream NO signaling. The chapter will present the cell types and cellular models (2D and 3D) available to study functional aspects of NO related strategies as well as the control of cell–cell interaction. By using selective biochemical inhibitors of signaling pathways, the involvement of intracellular messengers can be assessed and verified in functional responses both on cell cultures and in isolated organs. Finally, animal models reproducing human diseases or their symptoms can be used to assess the efficacy of synthetic strategies, NO delivery systems, and potential drugs or drug combinations in controlling pathology progression or in inducing disorder regression. Efficacy studies on experimental models, together with safety assessment, indeed allow to obtain predictive information for the proper design of safe human clinical trials
    corecore