Search Results - (Author, Cooperation:G. Fragoso)

Showing 1 - 4 results of 4, query time: 0.11s Refine Results
  1. 1
    Staff View
    Publication Date:
    2013-03-15
    Publisher:
    Nature Publishing Group (NPG)
    Print ISSN:
    0028-0836
    Electronic ISSN:
    1476-4687
    Topics:
    Biology
    Chemistry and Pharmacology
    Medicine
    Natural Sciences in General
    Physics
    Keywords:
    Adaptation, Physiological/*genetics ; Animals ; Biological Evolution ; Cestoda/drug effects/*genetics/physiology ; Cestode Infections/drug therapy/metabolism ; Conserved Sequence/genetics ; Echinococcus granulosus/genetics ; Echinococcus multilocularis/drug effects/genetics/metabolism ; Genes, Helminth/genetics ; Genes, Homeobox/genetics ; Genome, Helminth/*genetics ; HSP70 Heat-Shock Proteins/genetics ; Humans ; Hymenolepis/genetics ; Metabolic Networks and Pathways/genetics ; Molecular Targeted Therapy ; Parasites/drug effects/*genetics/physiology ; Proteome/genetics ; Stem Cells/cytology/metabolism ; Taenia solium/genetics
    Published by:
    http://www.nature.com/

    Latest Papers from Table of Contents or Articles in Press
  2. 2
    López-Colomé, A. M. ; Fragoso, G.
    Springer
    Published 1995
    Staff View
    ISSN:
    1573-6903
    Keywords:
    Glutamate receptors ; retina ; cell culture ; glycine ; taurine
    Source:
    Springer Online Journal Archives 1860-2000
    Topics:
    Medicine
    Notes:
    Abstract The effect of glycine (Gly) and taurine (Tau) on the biochemical and pharmacological properties of [3H]l-glutamate ([3H] Glu) binding to membranes from primary cultures of chick retinal pigment epithelium (RPE), as well as from intact tissue during development was studied. Gly and Tau increase Bmax of [3H]Glu binding to a high affinity site (KB=300 nM) in membranes from 16 days in vitro (immature) cultures; additionally, Gly discloses a low affinity Glu-binding site (KB=970 nM) at this stage. In membranes from 25 days in vitro (mature) cultures, the high affinity site is no longer present and Tau has no effect on Glu-binding; Gly still stimulates binding to the low affinity site by four fold, with an EC50=200 μM. Pharmacological profile using specific excitatory amino acid (EAA) receptor agonists and antagonists suggests that at 16 days in vitro Glu binds preferentially to metabotropic Glu receptors (mGluRs), and at 25 days in vitro to ionotropic receptors different from neuronal ones. The stimulatory effect of Gly and Tau was also observed in intact RPE, and decreased with increasing embryonic age. Glu binding was also stimulated in membranes from chick retina, but not in those from rat brain. Results support the possibility of EAA participation in several aspects of RPE physiology, including phagocytosis and cell division.
    Type of Medium:
    Electronic Resource
    URL:
    http://dx.doi.org/10.1007/BF00970733

    Articles: DFG German National Licenses
  3. 3
    López-Colomé, A. M. ; Ortega, A. ; Fragoso, G. ; Trueba, E.
    Springer
    Published 1997
    Staff View
    ISSN:
    1573-6903
    Keywords:
    Inositol phosphates ; radial glia ; cerebellum ; glutamate receptors
    Source:
    Springer Online Journal Archives 1860-2000
    Topics:
    Medicine
    Notes:
    Abstract Glutamate (L-glu) receptors coupled to phosphoinositide hydrolysis in primary cultures of Bergmann cells from chick cerebellum were characterized biochemically and pharmacologically. Both ionotropic and metabotropic receptor agonists stimulated [3H] inositol phosphates accumulation in the following order of potency: QA〉NMDA〉L-glu〉KA∼QA〉AMPA〉〉t-ACPD. QA showed a biphasic dose-response curve (EC50 = 0.07 and 53 μM), suggesting interaction with two populations of receptors; L-glu was the most efficient agonist. Stimulation by NMDA was blocked by CPP, APS and MK-801; that by AMP A and KA was inhibited 100% by CNQX and DNQX, whereas the effect of QA was decreased both by CNQX and the metabotropic antagonist 4-CPG. Stimulation of PIP2 hydrolysis induced by metabotropic L-glu receptor agonist t-ACPD was blocked by 4-CPG but was only moderately inhibited by MCPG. EAA-induced [3H]IPs accumulation was dependent on external Ca2+ and was not affected by nifedipine verapamil, or dantrolene; thapsigargin increased the effect. Results suggest that EAA activate the PI pathway in Bergmann glia through ionotropic (NMDA and AMPA/KA) as well as metabotropic receptor subtypes (t-ACPD) which could act jointly influencing neurotransmission at the parallel fiber—Purkinje cell synapses in the cerebellum.
    Type of Medium:
    Electronic Resource
    URL:
    http://dx.doi.org/10.1023/A:1022494923084

    Articles: DFG German National Licenses
  4. 4
    Staff View
    ISSN:
    1432-1955
    Source:
    Springer Online Journal Archives 1860-2000
    Topics:
    Biology
    Medicine
    Notes:
    Abstract Several inbred strains of mice were infected by intraperitoneal injection of tenTaenia crassiceps cysticerci per mouse. Genes linked with the major histocompatibility complex (H-2) were found to influence parasite growth greatly, as demonstrated by the different parasite loads of H-2 congenic mice with BALB background: BALB/c (H-2d) mice were the most susceptible, whereas BALB/k (H-2k) and BALB/b (H-2b) animals were comparatively resistant. Non-H-2 genes had no significant effect on susceptibility in H-2d strains, as reflected by the similar parasite loads in BALB/c, DBA/2, and (BALB/cxDBA/2)F1 mice. Using the H-2b (BALB/b, C57BL/6J) and H-2k (C3H/HeJ, BALB/k, and C3HeB/FeJ) strains, we found that non-H-2 background genes caused a small but significant influence on parasite load. A recombinant mouse strain alleles (Kk, Ik, Sd, Dd) was also susceptible, indicating that S and/or D regions of the H-2d complex are probably involved in the control of resistance to murine cysticercosis. Females of all mouse strains were more susceptible than males. The same effects were observed for H-2 genes and sex, with two strains ofT. crassiceps differing in their rate of growth.
    Type of Medium:
    Electronic Resource
    URL:
    http://dx.doi.org/10.1007/BF00930866

    Articles: DFG German National Licenses