Understanding Women With Advanced Gynecological Cancer: A Heideggerian Approach [compreendendo O Estar Com Câncer Ginecológico Avançado: Uma Abordagem Heideggeriana.]

This qualitative phenomenological research was carried out in order to understand how women experience living with advance gynecological cancer. We chose to make a qualitative survey in a phenomenological approach, based on the following directive question: "I'd like you to tell me your experience: 'How is it to be a woman with gynecological cancer?" ' Six women were interviewed. The ontological unification which emerged from the speeches were analyzed and interpreted according to Martin Heidegger's philosophical referential. These unifications made possible to see ways to care for these women that go far beyond technical and scientific knowledge. It is necessary to understand what has been lived by the other, thus ensuring a quality of care that contemplates subjectivity and inter-subjectivity.40225326

Measurement of the Bottom-Strange Meson Mixing Phase in the Full CDF Data Set

We report a measurement of the bottom-strange meson mixing phase \beta_s using the time evolution of B0_s -> J/\psi (->\mu+\mu-) \phi (-> K+ K-) decays in which the quark-flavor content of the bottom-strange meson is identified at production. This measurement uses the full data set of proton-antiproton collisions at sqrt(s)= 1.96 TeV collected by the Collider Detector experiment at the Fermilab Tevatron, corresponding to 9.6 fb-1 of integrated luminosity. We report confidence regions in the two-dimensional space of \beta_s and the B0_s decay-width difference \Delta\Gamma_s, and measure \beta_s in [-\pi/2, -1.51] U [-0.06, 0.30] U [1.26, \pi/2] at the 68% confidence level, in agreement with the standard model expectation. Assuming the standard model value of \beta_s, we also determine \Delta\Gamma_s = 0.068 +- 0.026 (stat) +- 0.009 (syst) ps-1 and the mean B0_s lifetime, \tau_s = 1.528 +- 0.019 (stat) +- 0.009 (syst) ps, which are consistent and competitive with determinations by other experiments.Comment: 8 pages, 2 figures, Phys. Rev. Lett 109, 171802 (2012

A glance at adenosine receptors: novel target for antitumor therapy.

Adenosine can be released from a variety of cells throughout the body, as the result of increased metabolic rates, in concentrations that can have a profound impact on the vasculature, immunoescaping, and growth of tumor masses. It is recognized that the concentrations of this nucleoside are increased in cancer tissues. Therefore, it is not surprising that adenosine has been shown to be a crucial factor in determining the cell progression pathway, either during apoptosis or during cytostatic state. From the perspective of cancer, the most important question then may be "Can activation and/or blockade of the pathways downstream of the adenosine receptor contribute to tumor development?" Rigorous examinations of the role of adenosine in in vivo and in vitro systems need to be investigated. The present review therefore proposes multiple adenosine-sustained ways that could prime tumor development together with the critical combinatorial role played by adenosine receptors in taking a choice between proliferation and death. This review proposes that adenosine acts as a potent regulator of normal and tumor cell growth. It is hypothesized that this effect is dependent on extracellular adenosine concentrations, cell surface expression of different adenosine receptor subtypes, and signal transduction mechanisms activated following the binding of specific agonists. We venture to suggest that the clarification of the role of adenosine and its receptors in cancer development may hold great promise for the treatment of chemotherapy in patients affected by malignancies

Modulation of metalloproteinase-9 in U87MG glioblastoma cells by A3 adenosine receptors.

In this work, we investigated the biological functions of adenosine (ado) in metalloproteinase-9 (MMP-9) regulation in U87MG human glioblastoma cells. The nucleoside was able to increase both MMP-9 mRNA and protein levels through A3 receptors activation. We revealed that A3 receptor stimulation induced an increase of MMP-9 protein levels in cellular extracts of U87MG cells by phosphorylation of extracellular signal-regulated protein kinases (ERK1/2), c-Jun N-terminal kinase/stress-activated protein kinase (pJNK/SAPK), protein kinase B (Akt/PKB) and finally activator protein 1 (AP-1). A3 receptor activation stimulated also an increase of extracellular MMP-9 in the supernatants from U87MG glioblastoma cells. Finally, the Matrigel invasion assay demonstrated that A3 receptors, by inducing an increase in MMP-9 levels, was responsible for an increase of glioblastoma cells invasion. Collectively, these results suggest that ado, through A3 receptors activation, modulates MMP-9 protein levels and plays a role in increasing invasion of U87MG cells

MODULATION OF MMP-9 IN U87MG GLIOBLASTOMA CELLS BY A3 ADENOSINE RECEPTORS

Adenosine (Ado) regulates a wide variety of physiological processes interacting with one or more of four known cell-surface receptors named A1, A2A, A2B and A3. The development of potent A3 agonists and selective antagonists revealed that the A3 subtype plays a pivotal role in the ado-induced modulation of tumor cells biology and the A3 subtype has been found up-regulated in cancer.1,2 Local invasive growth is one of the key features of primary brain tumors and metalloproteinases (MMPs) play a major role in promoting tumor metastasis. The involvement of ado in the regulation of MMP-9 in tumor cells have not been investigated by now. In this work, we investigated the biological functions of adenosine (ado) in metalloproteinase-9 (MMP-9) regulation in U87MG human glioblastoma cells. The nucleoside was able to increase both MMP-9 mRNA and protein levels through A3 receptors activation. We revealed that A3 receptor induced an increase of MMP-9 protein levels by phosphorylation of extracellular signal-regulated protein kinase (ERK1/2), c-Jun N-terminal kinase/stress-activated protein kinase (pJNK/SAPK), protein kinase B (Akt/PKB) and finally activator protein 1 (AP-1). A3 receptor activation stimulated also an increase of MMP-9 secretion and activity in supernatants from U87MG glioblastoma cells. Finally, the Matrigel invasion assay demonstrated that A3 receptors, by inducing an increase in MMP-9 levels, was responsible for an increase of glioblastoma cells invasion. Collectively, these results suggest for the first time that ado, through A3 receptors activation, modulates MMP-9 protein levels and plays a role in inducing invasion of U87MG cells. (1) Gessi, S.; Merighi, S.; Varani, K.; Leung, E.; Mac Lennan, S.; Borea, P.A. The A3 adenosine receptor: an enigmatic player in cell biology. Pharmacol. Ther. 2008, 117, 123-40. (2) Gessi, S.; Cattabriga, E.; Avitabile, A.; Gafa', R.; Lanza, G.; Cavazzini, L.; Bianchi, N.; Gambari, R.; Feo, C.; Liboni, A.; Gullini, S.; Leung, E.; Mac-Lennan, S.; Borea, P.A. Elevated expression of A3 adenosine receptors in human colorectal cancer is reflected in peripheral blood cells. Clin. Cancer Res. 2004, 10, 5895-901