71,995 research outputs found
Brush border inositol transport by intestines of carnivourus and herbivourus teleosts. Am. J. Physiol. 256: G501-G508.
No full textEvidence for the decay B0→J/ψω and measurement of the relative branching fractions of meson decays to J/ψη and J/ψη′
Get PDFFirst evidence of the B 0 → J / ψ ω decay is found and the B s 0 → J / ψ η and B s 0 → J / ψ η ′ decays are studied using a dataset corresponding to an integrated luminosity of 1.0 fb -1 collected by the LHCb experiment in proton-proton collisions at a centre-of-mass energy of sqrt(s) = 7 TeV. The branching fractions of these decays are measured relative to that of the B 0 → J / ψ ρ 0 decay:frac(B (B 0 → J / ψ ω), B (B 0 → J / ψ ρ 0)) = 0.89 ± 0.19 (stat) - 0.13 + 0.07 (syst),frac(B (B s 0 → J / ψ η), B (B 0 → J / ψ ρ 0)) = 14.0 ± 1.2 (stat) - 1.5 + 1.1 (syst) - 1.0 + 1.1 (frac(f d, f s)),frac(B (B s 0 → J / ψ η ′), B (B 0 → J / ψ ρ 0)) = 12.7 ± 1.1 (stat) - 1.3 + 0.5 (syst) - 0.9 + 1.0 (frac(f d, f s)), where the last uncertainty is due to the knowledge of f d / f s, the ratio of b-quark hadronization factors that accounts for the different production rate of B 0 and B s 0 mesons. The ratio of the branching fractions of B s 0 → J / ψ η ′ and B s 0 → J / ψ η decays is measured to befrac(B (B s 0 → J / ψ η ′), B (B s 0 → J / ψ η)) = 0.90 ± 0.09 (stat) - 0.02 + 0.06 (syst)
Hydrogen ion dynamics and the Na+/H+ exchanger in cancer angiogenesis and antiangiogenesis
No full textTumour angiogenesis and cellular pH regulation, mainly represented by Na+/H+ antiporter exchange, have been heretofore considered unrelated subfields of cancer research. In this short review, the available experimental evidence relating these areas of modern cancer research is introduced. This perspective also helps to design a new approach that facilitates the opening and development of novel research lines oriented towards a rational incorporation of anticancer drugs into more selective and less toxic therapeutic protocols. The final aim of these efforts is to control cancer progression and dissemination through the control of tumour angiogenesis. Finally, different antiangiogenic drugs that can already be clinically used to this effect are briefly presented
pH regulators in invadosomal functioning: Proton delivery for matrix tasting.
No full textInvadosomes are actin-rich finger-like cellular structures sensing and interacting with the surrounding extracellular matrix (ECM) and involved in its proteolytic remodeling. Invadosomes are structures distinct from other adhesion complexes, and have been identified in normal cells that have to cross tissue barriers to fulfill their function such as leukocytes, osteoclasts and endothelial cells. They also represent features of highly aggressive cancer cells, allowing them to escape from the primary tumor, to invade surrounding tissues and to reach systemic circulation. They are localized to the ventral membrane of cells grown under 2-dimensional conditions and are supposed to be present all around cells grown in 3-dimensional matrices. Indeed invadosomes are key structures in physiological processes such as inflammation and the immune response, bone remodeling, tissue repair, but also in pathological conditions such as osteopetrosis and the development of metastases. Invadosomes are subdivided into podosomes, found in normal cells, and into invadopodia specific for cancer cells. While these two structures exhibit differences in organization, size, number and half-life, they share similarities in molecular composition, participation in cell-matrix adhesion and promoting matrix degradation. A key determinant in invadosomal function is the recruitment and release of proteases, such as matrix metalloproteinases (MMPs), serine proteases and cysteine cathepsins, together with their activation in a tightly controlled and highly acidic microenvironment. Therefore numerous pH regulators such as V-ATPases and Na(+)/H(+) exchangers, are found in invadosomes and are directly involved in their constitution as well as their functioning. This review focuses on the participation of pH regulators in invadosome function in physiological and pathological conditions, with a particular emphasis on ECM remodeling by osteoclasts during bone resorption and by cancer cells
Resistance to antiangiogenic treatments: A review
No full textAngiogenesis (blood vessel formation) is essential for tissue growth in both normal development and physiology and in some diseases such as inflammation and cancer. Angiogenesis is a hallmark of cancer, however, it took many years to establish its importance. Ever since Judah Folkman’s seminal publications in 1971, that clearly showed cancer angiogenesis-dependence, researchers have been investigating the mechanisms of angiogenesis and how to block them. This search blossomed with the finding of inhibitors targeting the vascular endothelial growth factor (VEGF) signaling pathways. These new molecules and monoclonal antibodies showed therapeutic efficacy in both the laboratory and human clinical settings and hopes rose. Unfortunately, the benefits did not reach all the patients and they were short-lived: sooner or later tumors resumed their growth and proliferation and became refractory to further antiangiogenic treatments. Worse, antiangiogenic treatments seemed to increase metastatic risk. The development of treatment resistance is still one of the main causes of failure in cancer therapy. Antiangiogenic treatments are no exception and a deeper knowledge of the mechanisms of resistance is necessary if we intend to delay or eliminate them.Two different mechanisms have been identified: primary or evasive resistance and secondary or adaptive resistance.The existence of these two mechanisms led to the non-mainstream conclusion, now shared by many authors, that there are at least two different angiogenic pathways: one is the canonical VEGF- VEGF receptor (VEGFR) axis and others, which are independent of this axis and not fully known. Primary resistance works exclusively through these independent pathways, while secondary resistance, which initially is VEGF-VEGFR-dependent, switches to the other pathways becoming non-responsive to classical antiangiogenic treatments. For the time being, the clear identification of these other pathways belongs to the realm of hypothesis. However, there is enough experimental evidence supporting their existence. We will discuss this evidence as a central issue in antiangiogenic treatment resistance. Some non-conventional pharmacologic strategies against resistance will also be considered
Role of Stromal Cells in Determining Tumor and Cancer Stem Cell Behaviors and Therapeutic Response
No full textWhile research previously focused extensively on the tumor cells, over the last two decades, the tumor microenvironment (TME) has received increasing attention with a particular emphasis in its role in tumor development, metabolism, progression, and treatment response [...
Synergy between low dose metronomic chemotherapy and the pH-centered approach against cancer
No full textLow dose metronomic chemotherapy (MC) is becoming a mainstream treatment for cancer in veterinary medicine. Its mechanism of action is anti-angiogenesis by lowering vascular endothelial growth factor (VEGF) and increasing trombospondin-1 (TSP1). It has also been adopted as a compassionate treatment in very advanced human cancer. However, one of the main limitations of this therapy is its short-term effectiveness: 6 to 12 months, after which resistance develops. pH-centered cancer treatment (pHT) has been proposed as a complementary therapy in cancer, but it has not been adopted or tested as a mainstream protocol, in spite of existing evidence of its advantages and benefits. Many of the factors directly or indirectly involved in MC and anti-angiogenic treatment resistance are appropriately antagonized by pHT. This led to the testing of an association between these two treatments. Preliminary evidence indicates that the association of MC and pHT has the ability to reduce anti-angiogenic treatment limitations and develop synergistic anti-cancer effects. This review will describe each of these treatments and will analyze the fundamentals of their synergy
Measurement of the CP-violating phase \phi s in Bs->J/\psi\pi+\pi- decays
Get PDFMeasurement of the mixing-induced CP-violating phase phi_s in Bs decays is of prime importance in probing new physics. Here 7421 +/- 105 signal events from the dominantly CP-odd final state J/\psi pi+ pi- are selected in 1/fb of pp collision data collected at sqrt{s} = 7 TeV with the LHCb detector. A time-dependent fit to the data yields a value of phi_s=-0.019^{+0.173+0.004}_{-0.174-0.003} rad, consistent with the Standard Model expectation. No evidence of direct CP violation is found
Intestinal glucose transport and salinity adaptation in a euryhaline teleost
No full textGlucose transport by upper and lower intestinal brush-border membrane vesicles of the African tilapia (Oreochromis mossambicus) was characterized in fish acclimated to either freshwater or full-strength seawater. D-[3H]-glucose uptake by vesicles was stimulated by a transmembrane Na gradient, was electrogenic, and was enhanced by counter-transport of either D-glucose or D-galactose. Glucose transport was greater in the upper intestine than in the lower intestine and in seawater animals rather than in fish acclimated to freshwater. Glucose influx (10-s uptake) involved both saturable and nonsaturable transport components. Seawater adaptation increased apparent glucose influx K(t), J(max), apparent diffusional permeability (P), and the apparent Na affinity of the cotransport system in both intestinal segments, but the stoichiometry of Na-glucose transfer (1:1) was unaffected by differential saline conditions or gut region. It is suggested that increased sugar transport in seawater animals is due to the combination of enhanced Na-binding properties and an increase in number of transfer rate of the transport proteins. Freshwater animals compensate for reduced Na affinity of the coupled process by markedly increasing the protein affinity for glucose
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